Effects of MCI-186 on intracellular calcium ion concentration and membrane fluidity of hippocampal neurons in a rat model of Alzheimer's disease
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 l...
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Published in | 中国神经再生研究:英文版 Vol. 6; no. 29; pp. 2245 - 2250 |
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Main Author | |
Format | Journal Article |
Language | English |
Published |
2011
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Subjects | |
Online Access | Get full text |
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Summary: | 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. |
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Bibliography: | 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 Yu,Lei Qin,Zhao Wang,Xiaohong Lu,Ying Zhu,Wenhui Leng,Xuan Wang( 1.Department of Neurology, Affiliated Hospital of Jiangsu University, Zhenjiang 212001, Jiangsu Province, China; 2.Department of Preventive Medicine, Nanjing University of Chinese Medicine, Nanjing 210046, Jiangsu Province, China; 3.Department of Biochemistry, Basic Medical College of Jiamusi University, Jiamusi 154007, Heilongjiang Province, China; 4.Department of Neurology, Affiliated First Hospital of Jiamusi University, Jiamusi 154002, Heilongjiang Province, China;) MCI-186; Alzheimer's disease; learning; memory; calcium ion; neurodegenerative diseases; neural regeneration 11-5422/R |
ISSN: | 1673-5374 |