大鼠能量限制通过上调脂联素水平减轻脑缺血损伤

被引：2

作者：

李照菊

贾济

张丽娜

董海龙

熊利泽

机构：

[1] 第四军医大学西京医院麻醉科

来源：

中华神经外科疾病研究杂志 | 2012年 / 11卷 / 01期

基金：

国家自然科学基金重点项目;

关键词：

能量限制; 脂联素; 脑缺血耐受; 神经保护;

D O I：

暂无

中图分类号：

R743.3 [急性脑血管疾病（中风）];

学科分类号：

摘要：

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。

引用

页码：50 / 53

页数：4

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