The present study observed the effects of MCI-186 on the intracellular calcium ion concentration （[Ca2＋]i） and membrane fluidity of hippocampal neurons in Alzheimer＇s disease （AD） model rats to validate the neuroprotective effects of MCI-186. Compared with normal and sham-operated rats, the escape latency was obviously prolonged, spanning platform times were obviously reduced, [Ca2＋]i was increased, and microviscosity η value was increased in AD rats. MCI-186 at 0.5 mg/mL and 0.2 mg/mL obviously shortened escape latency, increased spanning platform times and decreased [Ca2＋]i and microviscosity η values in AD rats at 7 and 17 days after induction of the model. The differences in the above-mentioned indices between normal and MCI-186-treated rats were statistically significant. MCI-186 at 0.2 mg/mL yielded better curative effects than 0.5 mg/mL MCI-186. These findings suggest that MCI-186 improves learning and memory abilities in AD rats by decreasing [Ca2＋]i and increasing membrane fluidity of hippocampal neurons.
Ming YuLei QinZhao WangXiaohong LuYing ZhuWenhui LengXuan Wang
Oxidative stress has an important role in the development of Alzheimer＇s disease （AD）. Beta amyloid protein 25-35 （Aβ25-35） can generate oxygen free radicals, and MCI-186 （3-methyl-l-phenyl-2-pyrazolin-5-one, edaravone） can specifically eliminate hydroxyl radicals. The present study introduced Aβ25-35 into PC12 cells to establish a cell model of AD, and investigated the neuroprotective effects of MCI-186 on AD. Results showed that MCI-186 had a positive effect on the prevention and treatment of AD by inhibiting protein oxidative products, advanced glycation end products, lipid oxidative end products and DNA oxidative damage in PC12 cells induced by Aβ25-35.
Ming YuShujuan LiWenhui LengHan ChenYingquan WuLirong Yan
