大鼠能量限制通过上调脂联素水平减轻脑缺血损伤

Calorie restriction attenuates brain ischemia injury via increasing adiponectin synthesis in rats

目的能量限制(CR)可产生脑缺血耐受作用,但其详细机制尚不清楚。本研究主要探讨CR产生脑缺血耐受效应是否与脂联素(APN)合成水平有关。方法 SD大鼠分为两组:CR和自由饮食(AL)组。喂养4 w后,行大脑中动脉阻断模型(MCAO),检测MCAO前后大鼠血清及脑组织APN、内皮型一氧化氮合酶(eNOS)和一氧化氮(NO)含量,并测定大鼠脑梗死容积和神经功能评分,观察大鼠体内APN含量与CR产生脑缺血耐受间的关系。结果①MCAO后神经功能评分显示,CR组大鼠神经功能评分明显好于AL组(P<0.05);②MCAO后脑梗死容积测量结果显示,CR组大鼠脑梗死容积明显小于AL组(P<0.05);③经ELISA检测,CR可显著促进大鼠体内APN合成(与AL组比较P<0.05),并可增加MCAO后3h大鼠血清和脑内eNOS表达及NO含量(P<0.05)。结论 CR可能通过增加体内APN合成、上调eNOS表达和促进NO分泌产生脑缺血耐受效应。

Objective It is known that calorie restriction（CR） induces brain ischemic tolerance,while associated mechanism is still unclear.This study aims to investigate the relationship between adiponectin（APN） and brain ischemic tolerance induced by CR.Methods The SD rats were divided into two groups： calorie restriction（CR） group and ad libitum feeding（AL） groups.Following 4 weeks of feeding,the middle cerebral artery occlusion（MCAO） was conducted to induce transient focal ischemic stroke,and then APN,nitric oxide（NO） and endothelial nitric oxide synthase（eNOS） levels in serum and brain were measured via enzyme-linked immunosorbent assay（ELISA） assays at 24 h after MCAO.Neurological function scores and infarct volume were assessed to study the relationship between APN and brain ischemic tolerance induced by CR.ResultsNeurological function score of CR group was higher than that of AL group（P0.05）,and the brain infarct volume was improved markedly via CR in CR group compared to AL group（P0.05）.In comparison with the AL group,CR enhanced the synthesis of APN significantly（P0.05）,and increased NO and eNOS levels in the serum and brain at 3 h after MCAO（P0.05）.Conclusion CR induces brain ischemic tolerance in rats via increasing the synthesis of APN.