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【目的】探讨丹红注射液干预大鼠脑缺血再灌注损伤后热休克蛋白（Hsp ）20表达及意义。【方法】104只SD大鼠随机分为：8只正常对照（C组），未做任何处理；缺血再灌注损伤48只（I／R组），丹红注射液干预48只（DI／R组）。I／R组与DI／R组均采用大脑中动脉闭塞方法制作大鼠脑缺血再灌注模型，DI／R组从实验前一天开始腹腔注射丹红注射液（8 mL／kg ，Qd），直到各时间点（脑缺血2h再灌注后6h、24h、48h、72h、7d，每个时间点8只）处死，I／R组与DI／R组相同时间点注射生理盐水。比较I／R组与DI／R组脑梗死体积和各时间点神经功能缺损评分和 Hsp20阳性细胞数。【结果】I／R组脑梗死体积为（105．11±10．60）mm3，显著高于DI／R组（82．16±7．02）mm3，其差异有统计学意义（ P ＜0．05）。I／R组脑缺血再灌注后6 h神经功能缺损评分与DI／R组比较无显著性差异（P＞0．05），而在24h、48h、72h、7d时，I／R组的神经功能缺损评分显著高于DI／R组（P＜0．05），DI／R组缺血再灌注时间越长，神经功能缺损评分越低。正常对照组神经细胞中Hsp20阳性细胞很少；I／R组 Hsp20的表达6 h开始随时间增加，在72 h Hsp20表达达到高峰，7 d表达陡然减少；DI／R组 Hsp20阳性细胞数趋势同I／R组，且均显著高于I／R组相应的各时间点阳性细胞数（ P ＜0．05）。【结论】大鼠脑缺血再灌注损伤后丹红干预，其大鼠Hsp20的表达增加，脑缺血后损伤程度减轻。“,”[Objective] To explore the expression of Hsp20 and the protective role of Danhong Injection in rat brain tissue after cerebral ischemic reperfusion .[Methods] A rat model of cerebral ischemia‐reperfusion was established through the method of middle cerebral artery occlusion .A total of 104 healthy male Sprague‐Dawley (SD) rats were randomly divided into normal control ,ischemia reperfusion (I/R) and Danhong injec‐tion intervention (D I/R) groups .And I/R and D I/R groups were sub‐divided into cerebral infarction and im‐mumohistochemistry groups .The expression of Hsp20 in brain tissue was detected by immunohistochemistry at 6 ,24 ,48 and 72h and Day 7 after IR in I/R and D I/R groups .All neurological deficit scores were assessed before sacrificing .And the experimental results were analyzed with Spss17 .0 .[Results] The cerebral infarct size was markedly larger in I/R group than that in D I/R group (105 .11 ± 10 .60 vs 82 .16 ± 7 .02 mm3 ) .And the difference was statistically significant ( P <0 .05) .The level of Hsp20 was evidently up‐regulated at 6h and peaked at 72h in I/R group ( P < 0 .05) .And the level of Hsp20 was evidently up‐regulated in D I/R group ( P<0 .05) .The neurological deficit scores of D I/R group were better than those of I/R group .[Con‐clusion] After ischemia‐reperfusion injury ,Danhong Injection may up‐regulate the level of Hsp20 and reduce the extent of ischemic damage .