Tiền điều trị bằng điện châm tại huyệt Zusanli (ST36) làm giảm tình trạng viêm do lipopolysaccharide gây ra ở chuột nhờ ức chế sự xâm nhập của Ca2+ liên quan đến thụ thể cannabinoid CB2

Inflammation - Tập 42 - Trang 211-220 - 2018
Tao Chen1, Yong Xiong2, Man Long3, Dan Zheng1, Hui Ke1, Jun Xie2, Nina Yin1, Zebin Chen4
1Department of Anatomy, School of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan, China
2College of Acupuncture and Moxibustion, Hubei University of Chinese Medicine, Wuhan, China
3School of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan, China
4Hubei Provincial Collaborative Innovation Center of Preventive Treatment by Acupuncture and Moxibustion, Hubei University of Chinese Medicine, Wuhan, China

Tóm tắt

Trong nghiên cứu này, chúng tôi nhằm điều tra ảnh hưởng của việc tiền điều trị bằng điện châm (EA) tại huyệt Zusanli (ST36) đối với mô hình chuột gây độc tố nội sinh do lipopolysaccharide (LPS) và khám phá các cơ chế phân tử tiềm tàng. Chuột được điều trị bằng EA tại ST36 trong 7 ngày trước khi tiếp xúc với LPS. Hai giờ sau khi tiêm LPS, các mẫu như huyết thanh, mô huyệt địa phương và lách được thu thập và xử lý để điều tra bao gồm sản xuất cytokine, nồng độ canxi cytosol (Ca2+), sự xâm nhập Ca2+, biểu hiện thụ thể CB2 (CB2R) và tín hiệu TLR4/NF-κB. Kết quả của chúng tôi cho thấy tiền điều trị bằng EA đã làm giảm đáng kể sản xuất cytokine viêm do LPS gây ra, như TNF-α, IL-1β, và IL-6. EA cũng tăng cường biểu hiện CB2R, ức chế sự xâm nhập Ca2+ và vô hiệu hóa tín hiệu TLR4/NF-κB, dẫn đến giảm đáng kể nồng độ Ca2+. Quan trọng là, đối kháng CB2R AM630 đã loại bỏ hiệu ứng ức chế của EA tại ST36 đối với chuột nhiễm độc tố nội sinh, cho thấy CB2R có liên quan đến hiệu ứng chống viêm của EA. Tiền điều trị bằng EA có thể tăng cường biểu hiện CB2R, ức chế sự xâm nhập Ca2+ và vô hiệu hóa tín hiệu TLR4/NF-κB, điều này góp phần làm giảm tình trạng viêm do LPS gây ra ở chuột.

Từ khóa

#điện châm #huyệt Zusanli #lipopolysaccharide #viêm #thụ thể cannabinoid CB2

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Thông tin xuất bản

Inflammation

Tập 42

211-220

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