An AD-related neuroprotector rescues transformed rat retinal ganglion cells from CoCl₂-induced apoptosis.
Some ocular diseases characterized by apoptotic death of retinal ganglion cells (RGCs) and Alzheimer's disease (AD) are chronic neurodegenerative disorders and have similarities in neuropathology. Humanin (HN) is known for its ability to suppress neuronal death induced by AD-related insults. In present study, we investigated the neuroprotective effects of HN on hypoxia-induced toxicity in RGC-5 cells. Hypoxia mimetic compound cobalt chloride (CoCl₂) could increase the cell viability loss and apoptosis, whereas HN can significantly attenuate these effects. This finding may provide new therapeutics for the retinal neurodegenerative diseases targeting neuroprotection.
Department of Ophthalmology, Shengjing Hospital, China Medical University, Sanhao street 36, Heping district, Shenyang 110004, Liaoning Province, China.
Jie
J
Men
Xiaohui
X
Zhang
Yang
Y
Yang
Dianwen
D
Gao
D000544:Alzheimer Disease / Q000188:drug therapy / Q000473:pathology*; D000818:Animals; D016587:Antimutagenic Agents / Q000633:toxicity; D017209:Apoptosis / Q000187:drug effects*; D002461:Cell Line, Transformed; D003035:Cobalt / Q000633:toxicity*; D047908:Intracellular Signaling Peptides and Proteins / Q000494:pharmacology*; D018696:Neuroprotective Agents / Q000494:pharmacology*; D051381:Rats; D012165:Retinal Ganglion Cells / Q000187:drug effects / Q000473:pathology*
D016587:Antimutagenic Agents; D047908:Intracellular Signaling Peptides and Proteins; D018696:Neuroprotective Agents; C427211:humanin; D003035:Cobalt; C018021:cobaltous chloride