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Journal of Medicine and Pharmacy","Tạp chí Y Dược học Cần Thơ",{"EN":487,"VI":488},"\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">04\u002F10\u002F2015 Ministry of Information and Communications allowed Can Tho journal of medicine and pharmacy to operate (102 \u002FGP-BTTTT)\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">07\u002F16\u002F2015 Can Tho journal of medicine and pharmacy is internationally recognized: ISSN 2354-1210\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">In 2016, The journal has been included in the list of medical science journals by The State Council for professorship which is awarded a work score of 0-0.5 points for a published article.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Can Tho Journal of Medicine and Pharmacy welcome original works that haven’t been submitted or published in other medical journals. Posts must contain content related to one of the journal’s categories.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The content published\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The journal is divided into 3 categories:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Scientific research article: are valuable scientific works, which have been researched and accepted.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Overview of medicine, biology and pharmacy: serving the objective of continuing training in the fields of medicine, biology and pharmacy; to systematize classical and modern knowledge.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Update information on new knowledge about medicine, biology, pharmacy in the country and in the world.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Scope\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Publication and introduction of scientific research in the fields:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Medicine (internal medicine, surgery, pediatrics, obstetrics and gynecology, odonto-stomatology, laboratory, oncology, traditional medicine, nursing).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Biology (genetics, biotechnology).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">+ Pharmacology (pharmaceutics, drug quality analysis-control, synthetic pharmaceutical chemistry, biochemistry, pharmacognosy, botany, clinical pharmacy).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- To enhance the quality of undergraduate, postgraduate education, scientifically researching and meet the necessary treatment in hospital.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Introducing the updated domestic and oversea information about science technology to promote scientific research and exchanging technology in local, other universities.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">- Exchanging pharmaceutical and medical information for social health developing in the Mekong Delta and Vietnam.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">The object\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Postgraduate students, student of Can Tho University of Medicine and Pharmacy, scientists from schools, research institutes, hospitals, health centers, pharmaceutical companies of the Mekong Delta; other provinces and regions in Vietnam and other country.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Address\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Headquarters of Can Tho Journal of Medicine and Pharmacy, located Scientific Research and International Cooperation Office: 179 Nguyen Van Cu Street, An Khanh Ward, Ninh Kieu District, Can Tho City, Vietnam.\u003C\u002Fspan>\u003C\u002Fp>","\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Ngày 16\u002F7\u002F2015, Tạp chí Y Dược học Cần Thơ được cấp chỉ số quốc tế: ISSN 2354-1210.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 4\u002F2016, Tạp chí đã được Hội đồng Giáo sư ngành Y đưa vào danh sách các tạp chí khoa học Y học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Năm 2020 Tạp chí Y Dược học Cần Thơ đã được phê duyệt vào danh mục của các Hội đồng Giáo sư ngành Dược học được tính điểm công trình 0-0,5 điểm cho một bài báo đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ ra 12 số\u002Fnăm, 180-200 trang\u002Fsố.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Từ tháng 12\u002F2022 Tạp chí Y Dược học Cần Thơ là thành viên của hệ thống Crossref và từ tháng 01\u002F2023 tạp chí thực hiện bình duyệt online kín 2 chiều nhằm tăng tính minh bạch, tin cậy của các công trình nghiên cứu khoa học và đảm bảo tốt nhất chất lượng khoa học của bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ, mục đích và phạm vi của tạp chí\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tôn chỉ và mục đích hoạt động của tạp chí: xuất bản nhằm mục đích phổ biến kết quả từ các đề tài nghiên cứu khoa học; giao lưu trao đổi khoa học, chia sẻ kinh nghiệm, học tập, đồng thời cập nhật thông tin khoa học mới trong các lĩnh vực y, sinh, dược học trong và ngoài nước.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phạm vi của tạp chí: Tạp chí xuất bản được chia thành 3 chuyên mục: (i) Bài báo nghiên cứu khoa học là kết quả công trình nghiên cứu khoa học có giá trị đã được triển khai nghiên cứu, (ii) Bài tổng quan y, sinh, dược học: phục vụ mục tiêu đào tạo liên tục trong lĩnh vực y, sinh, dược học; nhằm hệ thống hóa những kiến thức kinh điển và hiện đại; (iii) Thông tin cập nhật kiến thức mới về y, sinh, dược học trong nước và trên thế giới.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Chính sách truy cập mở\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ áp dụng chính sách truy cập mở đối với các bài báo đã xuất bản đến với độc giả, nhằm mở rộng cơ hội tiếp cận các kết quả nghiên cứu chất lượng cao và tăng cường trao đổi kiến thức. Tạp chí đăng tải trực tuyến (miễn phí) toàn văn các bài báo được công bố trên website của Tạp chí (https:\u002F\u002Ftapchi.ctump.edu.vn).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đạo đức xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ cam kết tuân thủ đạo đức xuất bản phù hợp với các hướng dẫn và tiêu chuẩn của the Committee on Publication Ethics (COPE), tuân thủ các nguyên tắc của COPE’s Core Practices, Best Practices Guidelines for Journal Editors và Guidelines on Good Publication Practices.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Bản thảo bài báo chỉ được chấp nhận khi được tác giả chịu trách nhiệm chính cam kết các nội dung sau: Các nội dung của bản thảo chưa được đăng tải toàn bộ hoặc một phần ở các tạp chí khác; Tất cả các tác giả đều có đóng góp một cách đáng kể vào quá trình nghiên cứu hoặc chuẩn bị bản thảo và cùng chịu trách nhiệm về các nội dung của bản thảo; Tuân thủ các biện pháp đảm bảo đạo đức nghiên cứu (ví dụ thỏa thuận đồng ý tham gia nghiên cứu).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Cam kết bảo mật\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí cam kết thực hiện và tuân thủ các quy định của luật và các văn bản hướng dẫn liên quan đến bảo mật thông tin cá nhân trên không gian mạng. Các thông tin mà người dùng (tác giả, độc giả, biên tập viên, người phản biện) nhập vào các biểu mẫu trên Hệ thống Quản lý xuất bản trực tuyến của tạp chí chỉ được sử dụng vào các mục đích đã được tuyên bố rõ ràng và sẽ không được cung cấp cho bất kỳ bên thứ ba nào khác, hay dùng vào bất kỳ mục đích nào khác.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Phí gửi bài\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng bài: 1.000.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Lệ phí gửi đăng nhanh: 1.500.000đ\u002Fbài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với tác giả là cán bộ viên chức thuộc Trường Đại học Y Dược Cần Thơ thì được hỗ trợ 50% lệ phí gửi đăng bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Đối với sinh viên thực hiện đề tài nghiên cứu khoa học cấp trường được hỗ trợ 100% lệ phí đăng bài ( Tác giả gửi đính kèm “ Quyết định về việc giao tổ chức thực hiện đề tài nghiên cứu khoa học cấp Trường của sinh viên”).\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Hình thức nộp lệ phí:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Tiền mặt:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Nộp trực tiếp tại Phòng Tài chính - Kế toán, Trường Đại học Y Dược Cần Thơ, số 179 Nguyễn Văn Cừ, P. An Khánh, Q. Ninh Kiều, thành phố Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Chuyển khoản:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tên Tài khoản: Trường ĐHYD Cần Thơ, Số TK: 0111000115668, tại ngân hàng Vietcombank chi nhánh Cần Thơ.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Thời gian: Áp dụng từ ngày 01\u002F02\u002F2023.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">* Phí gửi bài không được hoàn trả khi bài viết bị từ chối hoặc tác giả xin rút bài viết.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Quy trình phản biện bài báo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tạp chí Y Dược học Cần Thơ thực hiện quy trình phản biện kín hai chiều nghiêm ngặt. Danh tính của những người phản biện không được tiết lộ cho các tác giả và ngược lại. Quy trình thẩm định bài báo đăng gồm các bước sau:\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tiếp nhận bản thảo\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Tác giả liên hệ gửi bản thảo đến Tạp chí qua hệ thống trực tuyến tại website: https:\u002F\u002Ftapchi.ctump.edu.vn. Hướng dẫn về cách đăng ký, gửi bài và chuẩn bị bản thảo được cung cấp trên website của Tạp chí.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sàng lọc sơ bộ\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Sau khi Tòa soạn nhận được bài báo của tác giả, Ban Thư ký sẽ tiến hành kiểm tra sơ bộ bài báo (các yêu cầu về nội dung và hình thức). Những bài báo không đúng quy cách hoặc có nội dung không phù hợp hoặc vi phạm bản quyền sẽ bị từ chối (Ban Thư ký thông báo phản hồi đến tác giả trong vòng 1 tuần). Những bài báo đủ điều kiện, được Ban Thư ký tòa soạn chuyển đến Ban Biên tập có cùng chuyên môn với nội dung bài báo để đề xuất người phản biện. Thời gian kể từ khi Ban Biên tập nhận bài báo đến khi đề xuất người phản biện bài báo chậm nhất là 5 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Vòng phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký gửi bài và yêu cầu phản biện đến 02 phản biện độc lập.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Các phản biện gởi nhận xét cho Ban Thư ký. Thời gian từ khi gửi bài cho phản biện đến khi nhận ý kiến của phản biện tối đa là 20 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xử ký kết quả phản biện\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Nếu ý kiến đồng ý cho đăng và không cần chỉnh sửa, Ban Thư ký tiếp tục đăng bài theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Nếu ý kiến đồng ý đăng và cần chỉnh sửa, Ban Thư ký sẽ thông tin đến tác giả chỉnh sửa theo yêu cầu của người phản biện. Thời gian chỉnh sửa và gửi lại kéo dài không quá 2 tuần, từ khi tác giả bài báo nhận được thông tin (Quá trình này có thể lặp lại tối đa 2 lần\u002F1 bài báo). Khi có sự thống nhất, đồng ý của người phản biện; bài báo được tiếp tục đăng theo qui trình.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Những bài báo có chất lượng không đạt yêu cầu, cả 2 phản biện không đồng ý cho đăng sẽ bị Tòa soạn từ chối đăng.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">Xuất bản\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">1. Ban Thư ký tổng hợp các bản thảo đã được tác giả hoàn thiện sau thẩm định trình Ban Biên tập xem xét, Tổng Biên tập phê duyệt, quyết định bài đăng theo các tiêu chí: sự phù hợp nội dung với tôn chỉ và mục đích, thể loại bài viết (ưu tiên các bài có bài có nghiên cứu chuyên sâu, hàm lượng khoa học cao), đóng góp mới bài báo, bài báo được ưu tiên đăng trong số gần nhất của Tạp chí theo thứ tự: tính thời sự, chất lượng bài báo và thời gian gửi bài.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">2. Ban Biên tập và Ban Thư ký biên tập bản thảo, chế bản, đọc rà soát lỗi. Thời gian hoàn thành từ 10-15 ngày.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">3. Ban Thư ký có trách nhiệm thông báo cho tác giả bài báo (bằng e-mail) về tình hình phê duyệt bài báo, thời gian, số kỳ, tập xuất bản bài báo theo qui định.\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>\u003Cp>\u003Cspan style=\"color: rgb(0, 0, 0);\">4. Danh sách bài báo theo số Tạp chí được in ấn và phát hành trong năm định kỳ được công bố chính thức trên website: https:\u002F\u002Ftapchi.ctump.edu.vn\u003C\u002Fspan>\u003C\u002Fp>\u003Cp>\u003Cbr>\u003C\u002Fp>",{"VOID":490},"wcQ1uqwAAAAJ","2023-05-30T08:17:21.868+00:00",[],[494],{"id":495,"createTime":28,"updateTime":28,"relativeEntities":496,"slug":28,"properties":497,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":507,"parentIds":508,"statistic":28},"6413896b-eca9-442b-a73f-182a58a0ce40",[],{"title":498,"address":501,"country":504,"abbreviation":505},{"EN":499,"VI":500},"Can Tho University of Medicine and Pharmacy","Trường Đại học Y Dược Cần Thơ",{"EN":502,"VI":503},"No 179, Nguyen Van Cu street, An Khanh ward, Ninh Kieu district, Can Tho city, Vietnam","Số 179, đường Nguyễn Văn Cừ, phường An Khánh, quận Ninh Kiều, thành phố Cần Thơ, Việt Nam",{"VOID":15},{"VOID":506},"ctump","http:\u002F\u002Fwww.ctump.edu.vn\u002F",[],[],"https:\u002F\u002Ftapchi.ctump.edu.vn\u002Findex.php\u002Fctump",{"impactFactor":32,"impactFactorByYear":512,"i10Index":32,"i10IndexLast5Year":32,"totalPublication":514,"totalPublicationByYear":515,"totalCitation":520,"totalCitationByYear":521,"totalCitationPerPublication":108,"totalCitationPerPublicationByYear":523,"hindexLast5Year":45,"hindex":45},{"2022":513,"2023":111,"2024":106},0.01,1556,{"2020":47,"2021":516,"2022":517,"2023":518,"2024":519,"2025":122},57,306,801,358,161,{"2021":146,"2022":280,"2023":522},99,{"2021":524,"2022":318,"2023":104},0.23,{"impactFactor":28,"impactFactorByYear":28,"i10Index":123,"i10IndexLast5Year":123,"totalPublication":526,"totalPublicationByYear":527,"totalCitation":526,"totalCitationByYear":528,"totalCitationPerPublication":40,"totalCitationPerPublicationByYear":531,"hindexLast5Year":49,"hindex":49},476,{"0":205,"2019":123,"2021":139,"2022":459,"2023":451,"2024":357,"2025":49,"2026":48},{"2021":42,"2022":123,"2023":161,"2024":529,"2025":360,"2026":530},136,83,{"2021":105,"2022":513,"2023":532,"2024":127,"2025":533,"2026":534},0.62,25.43,13.83,{"id":536,"createTime":537,"updateTime":382,"relativeEntities":538,"slug":539,"properties":540,"entityType":25,"verifyStatus":26,"verifyTime":28,"verifyNote":28,"languages":552,"translateLanguages":28,"viewCount":133,"subjectFields":553,"manageAffiliations":554,"indexDatabases":555,"url":556,"thumbnailPath":557,"statistic":558,"gsStatistic":594,"type":55,"analyzePriority":28},"6984a56a-db70-403b-9cc4-4013e1ceaffa","2023-05-09T06:47:40.346+00:00",[],"T%E1%BA%A1p%20ch%C3%AD%20Nghi%C3%AAn%20c%E1%BB%A9u%20n%C6%B0%E1%BB%9Bc%20ngo%C3%A0i",{"country":541,"issn":542,"title":544,"introduce":547,"gsId":550},{"VOID":15},{"VOID":543},"25252445",{"EN":545,"VI":546},"VNU Journal of Foreign Studies","Tạp chí Nghiên cứu nước ngoài",{"EN":548,"VI":549},"{\"ops\":[{\"insert\":\"\\n\\nThe \\n\"},{\"attributes\":{\"italic\":true},\"insert\":\"VNU Journal of Science\"},{\"insert\":\"\\n was established in 1985 for the publication of national and international research papers in all fields of natural sciences and technology, social sciences and humanities. 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Free radicals are formed disproportionately in diabetes by glucose oxidation, nonenzymatic glycation of proteins, and the subsequent oxidative degradation of glycated proteins. Abnormally high levels of free radicals and the simultaneous decline of antioxidant defense mechanisms can lead to damage of cellular organelles and enzymes, increased lipid peroxidation, and development of insulin resistance. These consequences of oxidative stress can promote the development of complications of diabetes mellitus. Changes in oxidative stress biomarkers, including superoxide dismutase, catalase, glutathione reductase, glutathione peroxidase, glutathione levels, vitamins, lipid peroxidation, nitrite concentration, nonenzymatic glycosylated proteins, and hyperglycemia in diabetes, and their consequences, are discussed in this review. In vivo studies of the effects of various conventional and alternative drugs on these biomarkers are surveyed. 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KC, 1993, Possible superoxide radical‐induced alteration of vascular reactivity in aortas from streptozotocin‐treated rats, J Pharmacol Exp Ther, 266, 992",{},{"id":28,"text":1187,"url":28,"identifiers":1188},"10.1016\u002F0891-5849(94)00202-U",{"doi":1187},{"id":28,"text":1190,"url":28,"identifiers":1191},"10.1016\u002F0076-6879(90)86093-B",{"doi":1190},{"id":28,"text":1193,"url":28,"identifiers":1194},"10.1016\u002F0006-2952(93)90124-F",{"doi":1193},{"id":28,"text":1196,"url":28,"identifiers":1197},"10.2337\u002Fdiabetes.40.3.344",{"doi":1196},{"id":28,"text":1199,"url":28,"identifiers":1200},"10.1016\u002F0014-5793(90)80974-N",{"doi":1199},{"id":28,"text":1202,"url":28,"identifiers":1203},"10.1042\u002Fbj2450243",{"doi":1202},{"id":28,"text":1205,"url":28,"identifiers":1206},"10.1016\u002F0014-5793(93)81706-6",{"doi":1205},{"id":28,"text":1208,"url":28,"identifiers":1209},"Tsai EC, 1994, Reduced plasma peroxyl radical trapping capacity and increased susceptibility of LDL to 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87",{},{"id":28,"text":1442,"url":28,"identifiers":1443},"10.1055\u002Fs-2007-1001693",{"doi":1442},{"id":28,"text":1445,"url":28,"identifiers":1446},"Garg MC, 1996, Effect of vitamin E supplementation on antioxidant status of diabetic rats, Med Sci Res, 24, 325",{},{"id":28,"text":1448,"url":28,"identifiers":1449},"10.1007\u002Fs001250050883",{"doi":1448},{"id":28,"text":1451,"url":28,"identifiers":1452},"10.1161\u002F01.HYP.35.2.655",{"doi":1451},{"id":28,"text":1454,"url":28,"identifiers":1455},"10.1076\u002Fceyr.21.4.814.5545",{"doi":1454},{"id":28,"text":1457,"url":28,"identifiers":1458},"10.1042\u002Fbj2560205",{"doi":1457},{"id":28,"text":1460,"url":28,"identifiers":1461},"10.1016\u002F0891-5849(91)90040-A",{"doi":1460},{"id":28,"text":1463,"url":28,"identifiers":1464},"10.1016\u002F0076-6879(84)06010-9",{"doi":1463},{"id":28,"text":1466,"url":28,"identifiers":1467},"10.1038\u002F414813a",{"doi":1466},{"id":28,"text":1469,"url":28,"identifiers":1470},"10.1016\u002FS0165-0173(96)00016-1",{"doi":1469},{"id":28,"text":1472,"url":28,"identifiers":1473},"Brownlee M, 1990, Diabetes Mellitus: Theory and Practice, 279",{},{"id":28,"text":1475,"url":28,"identifiers":1476},"10.1016\u002FS0898-6568(97)00131-9",{"doi":1475},{"id":28,"text":1478,"url":28,"identifiers":1479},"Aruna RV, 1999, Effect of betacarotene on protein glycosylation in alloxan induced diabetic rats, Indian J Exp Biol, 37, 399",{},{"id":28,"text":1481,"url":28,"identifiers":1482},"10.1097\u002F00005344-200008000-00017",{"doi":1481},{"id":28,"text":1484,"url":28,"identifiers":1485},"10.1089\u002Fjop.2000.16.149",{"doi":1484},{"id":28,"text":1487,"url":28,"identifiers":1488},"10.1002\u002F(SICI)1099-0461(1998)12:4\u003C219::AID-JBT4>3.0.CO;2-O",{"doi":1487},{"id":28,"text":1490,"url":28,"identifiers":1491},"Lu SC, 1997, Progressive defect in biliary GSH secretion in streptozotocin‐induced diabetic rats, Am J Physiol, 272, G374",{},{"id":28,"text":1493,"url":28,"identifiers":1494},"10.1007\u002FBF01081736",{"doi":1493},{"id":28,"text":1496,"url":28,"identifiers":1497},"Watkins JB, 1995, Diabetes mellitus‐induced alterations of hepatobiliary function, Pharmacol Rev, 47, 1",{},{"id":28,"text":1499,"url":28,"identifiers":1500},"10.1016\u002FS0167-4838(00)00276-4",{"doi":1499},false,{"id":1503,"createTime":1504,"updateTime":1504,"relativeEntities":1505,"slug":1506,"properties":1507,"entityType":1010,"verifyStatus":884,"verifyTime":1504,"verifyNote":1520,"languages":1521,"translateLanguages":28,"viewCount":32,"primaryUrl":1522,"fullTextUrl":28,"authors":1523,"publicationType":1073,"publisherRelationship":1581,"citationCount":684,"citationInfo":1652,"publishDate":1655,"publishYear":1653,"citationAnalyzeStatus":884,"lastCitationAnalyze":28,"indexDatabases":1656,"openAccess":28,"references":1657,"isForceReanalyzing":1501},"f1bfce5d-8ee5-440b-8069-37d558f474dd","2024-09-01T17:12:18.879+00:00",[],"Protective-effect-of-caffeic-acid-phenethyl-ester-CAPE-on-lipid-peroxidation-and-antioxidant-enzymes-in-diabetic-rat-liver",{"openalex":1508,"mag":1510,"abstract":1512,"title":1514,"pm":1516,"doi":1518},{"VOID":1509},"W2055869768",{"VOID":1511},"2055869768",{"EN":1513},"\u003Cjats:title>Abstract\u003C\u002Fjats:title>\u003Cjats:p>The aim of this study was to examine the effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation (LPO) and the activities of antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH‐Px) in the liver of streptozotocin (STZ)‐induced diabetic rats. Twenty‐seven rats were randomly divided into three groups: group I, control non‐diabetic rats (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 9); group II, STZ‐induced, untreated diabetic rats (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 8); group III, STZ‐induced, CAPE‐treated diabetic rats (\u003Cjats:italic>n\u003C\u002Fjats:italic> = 10), which were intraperitoneally injected with CAPE (10 μM kg\u003Cjats:sup>−1\u003C\u002Fjats:sup> day\u003Cjats:sup>−1\u003C\u002Fjats:sup>) after 3 days followed by STZ treatment. The liver was excised after 8 weeks of CAPE treatment, the levels of malondialdehyde (MDA) and the activities of SOD, CAT, and GSH‐Px in the hepatic tissues of all groups were analyzed. In the untreated diabetic rats, MDA markedly increased in the hepatic tissue compared with the control rats (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.0001). However, MDA levels were reduced to the control level by CAPE. The activities of SOD, CAT, and GSH‐Px in the untreated diabetic group were higher than that in the control group (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.0001). The activities of SOD and GSH‐Px in the CAPE‐treated diabetic group were higher than that in the control group (respectively, \u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.0001, \u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.035). There were no significant differences in the activity of CAT between the rats of CAPE‐treated diabetic and control groups. Rats in the CAPE‐treated diabetic group had reduced activities of SOD and CAT in comparison with the rats of untreated diabetic group (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.0001). There were no significant differences in the activity of GSH‐Px between the rats of untreated diabetic and CAPE‐treated groups. It is likely that STZ‐induced diabetes caused liver damage. In addition, LPO may be one of the molecular mechanisms involved in STZ‐induced diabetic damage. CAPE can reduce LPO caused by STZ‐induced diabetes. © 2004 Wiley Periodicals, Inc. J Biochem Mol Toxicol 18:234–238, 2004; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002\u002Fjbt.20028\u003C\u002Fjats:p>",{"EN":1515},"Protective effect of caffeic acid phenethyl ester (CAPE) on lipid peroxidation and antioxidant enzymes in diabetic rat liver",{"VOID":1517},"15452882",{"VOID":1519},"10.1002\u002Fjbt.20028","Author affiliation is blank",[31],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fjbt.20028",[1524,1541,1552,1561,1570],{"id":1525,"sortIndex":32,"researcher":28,"roles":1526,"affiliations":1527,"properties":1536,"displayName":1538,"givenName":28,"familyName":28},"2794ffd8-6fc4-4180-a1f9-8b7d9086d7e8",[],[1528],{"id":1529,"sortIndex":32,"affiliation":1530,"properties":28},"bc211b6f-ae89-42d8-9569-36741946d1ac",{"id":1529,"createTime":28,"updateTime":28,"relativeEntities":1531,"slug":28,"properties":1532,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":1535,"statistic":28},[],{"title":1533},{"EN":1534},"Department of Medical 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Harmful effect of cadmium on testis is known to be germ cell degeneration and impairment of testicular steroidogenesis. In the present study, the effect of diallyl sulfide (DAS), a sulfur‐containing volatile compound present in garlic, and zinc (Zn) was investigated on cadmium‐induced testicular toxicity in rats. Male adult Wistar rats treated with cadmium (2.5 mg\u002Fkg body wt, five times a week for 4 weeks) showed decreased body weight, paired testicular weight, relative testicular weight, serum testosterone, luteinizing hormone, follicle‐stimulating hormone, and testicular total antioxidant capacity (TAC) and protein levels. Testicular steroidogenic enzymes, such as 3β‐hydroxysteroid dehydrogenase (3β‐HSD) and 17β‐hydroxysteroid dehydrogenase (17β‐HSD), and marker enzymes, such as sorbitol dehydrogenase (SDH), lactate dehydrogenase (LDH), acid phosphatase (ACP), alkaline phosphatase (ALP), and glucose‐6‐phosphate dehydrogenase (G6PD), showed a significant decrease in activities whereas that of γ‐glutamyl transferase was significantly increased after cadmium exposure. The results have revealed that concurrent treatment with DAS or zinc restored key steroidogenic enzymes, SDH, LDH, and G6PD and increased testicular weight significantly. DAS restored the TAC level and increased testosterone level and relative testicular weight significantly. Zinc restored testicular protein level and body weight. It can be concluded that cadmium causes testicular toxicity and inhibits androgen production in adult male rats probably by affecting pituitary gonadotrophins and that concurrent administration of DAS or zinc provides protection against cadmium‐induced testicular toxicity. © 2008 Wiley Periodicals, Inc. J Biochem Mol Toxicol 22:345–353, 2008; Published online in Wiley InterScience (\u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" xlink:href=\"http:\u002F\u002Fwww.interscience.wiley.com\">www.interscience.wiley.com\u003C\u002Fjats:ext-link>). 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study evaluates the protective effects of thymol on altered plasma lipid peroxidation products and nonenzymic antioxidants in isoproterenol (ISO)‐induced myocardial infarcted rats. Male albino Wistar rats were pre and cotreated with thymol (7.5 mg\u002Fkg body weight) daily for 7 days. ISO (100 mg\u002Fkg body weight) was subcutaneously injected into rats on 6th and 7th day to induce myocardial infarction (MI). Increased activity\u002Flevels of serum creatine kinase‐MB (CK‐MB), plasma thiobarbituric acid reactive substances, lipid hydroperoxides, and conjugated dienes with decreased levels of plasma reduced glutathione (GSH), vitamin C, and vitamin E were observed in ISO‐induced myocardial infarcted rats. Pre and cotreatment with thymol (7.5 mg\u002Fkg body weight) showed normalized activity of serum CK‐MB and near normalized levels of plasma lipid peroxidation products, reduced GSH, vitamin C, and vitamin E in myocardial infarcted rats. Furthermore, the in vitro study on reducing power of thymol confirmed its potent antioxidant action. Thus, thymol protects ISO‐induced MI in rats by its antilipid peroxidation and antioxidant properties. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:368–373, 2012; View this article online at \u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" xlink:href=\"wileyonlinelibrary.com\">wileyonlinelibrary.com\u003C\u002Fjats:ext-link>. DOI 10.1002\u002Fjbt.21431\u003C\u002Fjats:p>",{"EN":2570},"Protective effects of thymol on altered plasma lipid peroxidation and nonenzymic antioxidants in isoproterenol‐induced myocardial infarcted rats",{"VOID":2572},"22890907",{"VOID":2574},"10.1002\u002Fjbt.21431",[31],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fjbt.21431",[2578,2597],{"id":2579,"sortIndex":32,"researcher":28,"roles":2580,"affiliations":2581,"properties":2590,"displayName":2594,"givenName":28,"familyName":28},"df516c32-0750-4229-9164-7c14ed5162cb",[],[2582],{"id":2583,"sortIndex":32,"affiliation":2584,"properties":28},"e902d3b5-cad3-4a68-adae-01f89925ff00",{"id":2583,"createTime":28,"updateTime":28,"relativeEntities":2585,"slug":28,"properties":2586,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2589,"statistic":28},[],{"title":2587},{"VI":2588},"Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar—608 002, Tamil Nadu, India",[],{"orcid":2591,"title":2593,"openalex":2595},{"VOID":2592},"https:\u002F\u002Forcid.org\u002F0000-0001-6863-7372",{"EN":2594},"Mohamed Fizur Nagoor Meeran",{"VOID":2596},"A5070454315",{"id":2598,"sortIndex":40,"researcher":28,"roles":2599,"affiliations":2600,"properties":2607,"displayName":2611,"givenName":28,"familyName":28},"df185e4e-ff03-42fb-baa7-fa120873dd13",[],[2601],{"id":2583,"sortIndex":32,"affiliation":2602,"properties":28},{"id":2583,"createTime":28,"updateTime":28,"relativeEntities":2603,"slug":28,"properties":2604,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":2606,"statistic":28},[],{"title":2605},{"VI":2588},[],{"orcid":2608,"title":2610,"openalex":2612},{"VOID":2609},"https:\u002F\u002Forcid.org\u002F0000-0002-6840-4074",{"EN":2611},"P. 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flavonoids intake has been reported inversely related to the incidence of cardiovascular diseases (CVD). The present study is undertaken to evaluate the preventive role of naringin on mitochondrial enzymes in isoproterenol (ISO)‐induced myocardial infarction in male albino Wistar rats. Rats subcutaneously injected with ISO (85 mg\u002Fkg) at an interval of 24 h for 2 days, resulting in significant (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05) increase in the levels of mitochondrial lipid peroxides. ISO‐induction also showed significant (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05) decrease in the activities of mitochondrial tricarboxylic acid cycle enzymes (isocitrate dehydrogenase, succinate dehydrogenase, malate dehydrogenase, and α‐ketoglutarate dehydrogenase) and respiratory chain enzymes (NADH dehydrogenase and cytochrome c oxidase). Oral pretreatment with naringin (10, 20, and 40 mg\u002Fkg) to ISO‐induced rats daily for a period of 56 days significantly (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05) minimized the alterations in all the biochemical parameters and restored the normal mitochondrial function. Transmission electron microscopic (TEM) observations also correlated with these biochemical findings. Thus, our findings demonstrate that naringin prevents the mitochondrial dysfunction during ISO‐induced myocardial infarction in rats. © 2007 Wiley Periodicals, Inc. J Biochem Mol Toxicol 21:354–361, 2007; Published online in Wiley InterScience (\u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" xlink:href=\"http:\u002F\u002Fwww.interscience.wiley.com\">www.interscience.wiley.com\u003C\u002Fjats:ext-link>). 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Cisplatin induced a significant reduction in testicular weights, plasma testosterone, and testicular reduced glutathione levels in addition to a significant elevation of testicular malondialdehyde levels and testicular gene expressions of inducible nitric oxide synthase (iNOS), tumor necrosis factor‐α (TNF‐α), and p38 mitogen‐activated protein kinase (MAPK) when compared with the control group (\u003Cjats:italic>p\u003C\u002Fjats:italic> < 0.05). Lower tubular diameters and depletion of germ cells and irregular small seminiferous tubules with Sertoli cells only were observed in the cisplatin group. Arjunolic acid administration significantly corrected the changes in both biochemical and histopathological parameters. 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(\u003Cjats:styled-content style=\"fixed-case\">QT\u003C\u002Fjats:styled-content>), a dietary‐derived flavonoid, is ubiquitous in fruits and vegetables and plays an important role in human health by virtue of its antioxidant function. The present study was designed to examine the effects of \u003Cjats:styled-content style=\"fixed-case\">QT\u003C\u002Fjats:styled-content> on oxidative damage that was induced by the herbicide, atrazine (\u003Cjats:styled-content style=\"fixed-case\">ATZ\u003C\u002Fjats:styled-content>), in mixed cultures of Sertoli‐germ cells. Results showed that treatment with \u003Cjats:styled-content style=\"fixed-case\">QT\u003C\u002Fjats:styled-content> increased cell viability and decreased catalase activity, malondialdehyde, and reactive oxygen species (\u003Cjats:styled-content style=\"fixed-case\">ROS\u003C\u002Fjats:styled-content>) levels. \u003Cjats:styled-content style=\"fixed-case\">QT\u003C\u002Fjats:styled-content> treatment also increased the m\u003Cjats:styled-content style=\"fixed-case\">RNA\u003C\u002Fjats:styled-content> expression of glutathione peroxidase (\u003Cjats:styled-content style=\"fixed-case\">GSH\u003C\u002Fjats:styled-content>‐\u003Cjats:styled-content style=\"fixed-case\">P\u003C\u002Fjats:styled-content>x), glutathione reductase (\u003Cjats:styled-content style=\"fixed-case\">GR\u003C\u002Fjats:styled-content>), glutathione‐S‐transferase, and superoxide dismutase‐1 and could not reversed to the control levels \u003Cjats:styled-content style=\"fixed-case\">ATZ\u003C\u002Fjats:styled-content>‐induced steady‐state m\u003Cjats:styled-content style=\"fixed-case\">RNA\u003C\u002Fjats:styled-content> levels of these antioxidant genes as well as the level of glutathione and activities of \u003Cjats:styled-content style=\"fixed-case\">GSH\u003C\u002Fjats:styled-content>‐\u003Cjats:styled-content style=\"fixed-case\">P\u003C\u002Fjats:styled-content>x and \u003Cjats:styled-content style=\"fixed-case\">GR\u003C\u002Fjats:styled-content>. \u003Cjats:styled-content style=\"fixed-case\">QT\u003C\u002Fjats:styled-content> has protective effect against \u003Cjats:styled-content style=\"fixed-case\">ATZ\u003C\u002Fjats:styled-content>‐induced oxidative stress through a reduction in \u003Cjats:styled-content style=\"fixed-case\">ROS\u003C\u002Fjats:styled-content> levels and lipid peroxidation. © 2012 Wiley Periodicals, Inc. J Biochem Mol Toxicol 26:477‐485, 2012; View this article online at \u003Cjats:ext-link xmlns:xlink=\"http:\u002F\u002Fwww.w3.org\u002F1999\u002Fxlink\" xlink:href=\"http:\u002F\u002Fwww.wileyonlinelibrary.com\">wileyonlinelibrary.com\u003C\u002Fjats:ext-link>. DOI 10:1002\u002Fjbt.21449\u003C\u002Fjats:p>",{"EN":3247},"Dietary Antioxidant, Quercetin, Protects Sertoli‐Germ Cell Coculture from Atrazine‐Induced Oxidative Damage",{"VOID":3249},"23132811",{"VOID":3251},"10.1002\u002Fjbt.21449",[31],"https:\u002F\u002Fonlinelibrary.wiley.com\u002Fdoi\u002F10.1002\u002Fjbt.21449",[3255,3274,3293],{"id":3256,"sortIndex":32,"researcher":28,"roles":3257,"affiliations":3258,"properties":3267,"displayName":3271,"givenName":28,"familyName":28},"4f9f951f-8b97-40ff-b885-9f31eab2a793",[],[3259],{"id":3260,"sortIndex":32,"affiliation":3261,"properties":28},"1a3fae4a-e5ea-4194-8f04-e16096173dca",{"id":3260,"createTime":28,"updateTime":28,"relativeEntities":3262,"slug":28,"properties":3263,"entityType":28,"verifyStatus":28,"verifyTime":28,"verifyNote":28,"languages":28,"translateLanguages":28,"viewCount":28,"url":28,"parentIds":3266,"statistic":28},[],{"title":3264},{"VI":3265},"Department of Chemical Sciences, College of Natural Sciences, Redeemer’s University, Redemption City, Ogun State, Nigeria",[],{"orcid":3268,"title":3270,"openalex":3272},{"VOID":3269},"https:\u002F\u002Forcid.org\u002F0000-0003-3378-2689",{"EN":3271},"Sunny O. 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Previous studies have reported that mitochondrial transplantation provided surprising results in myocardial and liver ischemia, as well as in Parkinson's disease. We aimed to investigate the beneficial effects of isolated mitochondria transplantation from mesenchymal stem cells (MSCs) in vivo, to mitigate renal damage that arises from doxorubicin‐mediated nephrotoxicity and its action mechanism. In this study, a kidney model of doxorubicin‐mediated nephrotoxicity was used and isolated mitochondria from MSCs were transferred to the renal cortex of rats. The findings showed that the rate of isolated mitochondria from MSCs maintains sufficient membrane integrity, and was associated with a beneficial renal therapeutic effect. Following doxorubicin‐mediated renal injury, isolated mitochondria or vehicle infused into the renal cortex and rats were monitored for five days. This study found that mitochondrial transplantation decreased cellular oxidative stress and promoted regeneration of tubular cells after renal injury (\u003Cjats:italic>P\u003C\u002Fjats:italic> < .001, \u003Cjats:italic>P\u003C\u002Fjats:italic> = .009). Moreover, mitochondrial transplantation reduced protein accumulation of tubular cells and reversed renal deficits (\u003Cjats:italic>P\u003C\u002Fjats:italic> = .01, \u003Cjats:italic>P\u003C\u002Fjats:italic> < .001). Mitochondrial transplantation increased Bcl‐2 levels, and caspase‐3 levels decreased in injured renal cells (\u003Cjats:italic>P\u003C\u002Fjats:italic> < .015, \u003Cjats:italic>P\u003C\u002Fjats:italic> < .001). Our results provide a direct link between mitochondria dysfunction and doxorubicin‐mediated nephrotoxicity and suggest a therapeutic effect of transferring isolated mitochondria obtained from MSCs against renal injury. 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