Một tác nhân neuroprotection liên quan đến bệnh Alzheimer cứu sống các tế bào hạch võng mạc chuột chuyển hóa khỏi sự apoptosis do CoCl2 gây ra

Springer Science and Business Media LLC - Tập 47 - Trang 144-149 - 2012
Jie Men1, Xiaohui Zhang2, Yang Yang1, Dianwen Gao1
1Department of Ophthalmology, Shengjing Hospital, China Medical University, Shenyang, China
2Department of Ophthalmology, Harbin 242 Hospital, Harbin, China

Tóm tắt

Một số bệnh lý mắt đặc trưng bởi cái chết tế bào apoptosis của các tế bào hạch võng mạc (RGCs) và bệnh Alzheimer (AD) là những rối loạn thoái hóa thần kinh mạn tính và có nhiều điểm tương đồng trong bệnh lý thần kinh. Humanin (HN) được biết đến với khả năng ức chế cái chết tế bào dây thần kinh do các yếu tố liên quan đến bệnh AD gây ra. Trong nghiên cứu này, chúng tôi đã khảo sát tác dụng neuroprotective của HN đối với sự độc hại do thiếu oxy gây ra trong các tế bào RGC-5. Hợp chất mô phỏng thiếu oxy, clorua cobalt (CoCl2) có thể làm gia tăng sự mất khả năng sống của tế bào và apoptosis, trong khi HN có khả năng làm giảm đáng kể các tác động này. Phát hiện này có thể cung cấp các liệu pháp mới cho các bệnh thoái hóa thần kinh của võng mạc nhắm vào neuroprotection.

Từ khóa

#bệnh lý mắt #tế bào hạch võng mạc #bệnh Alzheimer #neuroprotection #hồi phục tế bào #apoptosis #thiếu oxy

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