Nội dung được dịch bởi AI, chỉ mang tính chất tham khảo
Peptid lõi hexapeptid amyloid-β N-tận cùng bảo vệ hiệu quả, đảo ngược tăng sinh tế bào thần kinh phản ứng và độc tính thần kinh trong các mô hình bệnh lý Alzheimer
Tóm tắt
Bệnh Alzheimer (AD) là một rối loạn thoái hóa thần kinh tiến triển, đặc trưng bởi sự tích tụ của amyloid beta (Aβ) ngoại bào và mạng lưới neurofibrillary nội bào, dẫn đến sự kích hoạt mãn tính của astrocytes và microglia và tình trạng viêm thần kinh dai dẳng. Sự kích hoạt của microglia và astrocytes liên quan đến Aβ dẫn đến tăng nồng độ canxi nội bào và sản xuất cytokine tiền viêm, tác động đến sự tiến triển của thoái hóa thần kinh. Một đoạn Aβ N-terminal (Aβ1–15) và một chuỗi lõi hexapeptid ngắn trong đoạn N-Aβ (N-Aβcore: Aβ10–15) đã được chứng minh trước đó có thể bảo vệ chống lại sự rối loạn chức năng ty thể do Aβ gây ra, căng thẳng oxy hóa và apoptosis ở tế bào thần kinh cũng như phục hồi các khiếm khuyết trí nhớ synaptic và không gian trong mô hình chuột APP/PSEN1. Ở đây, chúng tôi giả thuyết rằng đoạn N-Aβ và N-Aβcore có tác dụng bảo vệ chống lại độc tính gliotoxic do Aβ gây ra, thúc đẩy một môi trường bảo vệ thần kinh và có thể giảm nhẹ tình trạng viêm thần kinh dai dẳng đặc trưng trong AD. Chúng tôi đã điều trị các mẫu cắt não kiểu hình từ mô hình chuột AD gia đình già tuổi, 5xFAD, bằng N-Aβcore và sử dụng hóa miễn dịch tế bào để đánh giá tác động lên sự gia tăng astrocytes và microgliosis cũng như những thay đổi trong các điểm hạt synaptophysin tích cực được nuốt bởi microglia. Các nền văn hóa tế bào neuron/glia tách biệt, văn hóa glial hỗn hợp hoặc dòng tế bào microglia đã được điều trị bằng Aβ oligomeric người với nồng độ bắt chước nồng độ gây bệnh (μM) được quan sát trong AD trong điều kiện không có hoặc có sự hiện diện của các đoạn Aβ N-terminal không độc. Những thay đổi kết quả trong mật độ synaptic, gliosis, stress oxy hóa, rối loạn chức năng ty thể, apoptosis và sự biểu hiện và giải phóng của các dấu hiệu tiền viêm sau đó được xác định. Chúng tôi đã chứng minh rằng các đoạn Aβ N-terminal làm giảm chỉnh biến hình ảnh dẫn đến sự gia tăng astrocytes và microgliosis do nồng độ Aβ bệnh lý trong các nền văn hóa glial hỗn hợp và các mẫu cắt não kiểu hình từ mô hình chuột transgenic 5xFAD, trong khi bảo vệ chống lại stress oxy hóa, rối loạn chức năng ty thể và apoptosis do Aβ gây ra trong astrocytes và microglia tách biệt. Hơn nữa, việc bổ sung N-Aβcore đã làm giảm sự biểu hiện và giải phóng các chất trung gian tiền viêm trong các tế bào microglia bị kích hoạt bởi Aβ và phục hồi sự mất mát các yếu tố synaptic do Aβ gây ra. Tất cả những phát hiện này cho thấy chức năng bảo vệ của các đoạn Aβ N-terminal mở rộng đến tăng sinh gliosis và độc tính gliotoxic do Aβ gây ra, thông qua việc ngăn chặn hoặc đảo ngược các trạng thái phản ứng của glia biểu thị tình trạng viêm thần kinh và mất synaptic là trọng tâm của bệnh sinh AD.
Từ khóa
#Alzheimer #amyloid beta #N-terminal Aβ #neuroprotection #gliosis #neuroinflammationTài liệu tham khảo
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