目的：探讨红景天苷对大鼠脑缺血再灌注的保护作用及其分子机制。方法：SD大鼠随机分为4组：正常对照组、正常对照＋红景天苷组、脑缺血再灌注组、脑缺血再灌注＋红景天苷组。红景天苷处理组运用红景天苷（40 m g／kg ）处理2周，脑缺血再灌注采用局灶性脑缺血1 h ，随后再灌注24 h处理，随后取脑，测定脑缺血体积、检测MDA和8‐OHdG等应激产物，提取mRNA用于定量RT‐PCR测定基因表达水平变化。结果：正常对照＋红景天苷组大鼠的脑组织中 HIF‐1a、乳酸脱氢酶（LDH）和己糖激酶（HK）等表达水平显著升高。脑缺血再灌注可诱导 HIF‐1a、LDH和 HK的表达，红景天苷处理组行脑缺血再灌注后 HIF‐1a、LDH、HK升高程度较脑缺血再灌注组显著减弱。结论：红景天苷处理可诱导脑组织中 HIF‐1的表达，增加糖酵解酶的水平，加强脑组织对缺血再灌注损伤的抵抗。%Objective:To confirm the protective effects of salidroside on cerebral ischemia/reperfusion (I/R) injury and explore its molecular mechanism .Methods :SD rats were randomly divided into four groups:normal control ,normal rats+salidroside ,I/R group ,I/R +salidroside .Rats in groups with salidroside treatment were giv‐en salidroside (40 mg/kg) for two weeks .I/R rats were treated by the thread ligation in internal carotid artery .In the end of treatment ,the brain of each rat was collected .The infarct sizes ,the levels of malondialdehyde (MDA) and 8‐dydroxy‐2’‐deoxyguanosine (8‐O HdG ) in brain tissues ,and the expression of HIF‐1a , lactate dehydrogenase (LDH) and hexokinase (HK) were observed .Results :Salidroside treatment of normal rats induced a significant in‐crease in the expression of HIF‐1a ,LDH ,HK as compared to normal control .I/R resulted in the increase in the ex‐pression of HIF‐1a ,LDH ,HK as compared to normal control .Rats in I/R+ salidroside group had a significantly weakened increase in expression of HIF‐1a ,LDH ,HK as compared to I/R group .Infarct sizes were significantly smaller and levels of MAP and 8‐OHdG were significantly lower in I/R+salidroside group than those in I/R group . Conclusion :Salidroside induces cerebral HIF‐1a expression and increase enzyme levels for glucolysis ,which showed protective effects against cerebral ischemia reperfusion injury .
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