依达拉奉预处理对大鼠脑缺血再灌注海马细胞凋亡及bcl-2、bax表达的影响

目的观察依达拉奉预处理对脑缺血再灌注后神经细胞凋亡及bcl-2、Bax表达的影响。方法将45只健康雄性sD大鼠随机分为假手术组、生理盐水对照组、依达拉奉预处理组，各15只。采用线栓法制作大鼠大脑中动脉缺血模型，脑缺血再灌注前12h，预处理组给予依达拉奉3mg／kg，对照组给予等量生理盐水分别腹腔注射。脑缺血再灌注24h后断头取脑，应用免疫组织化学法及原位细胞凋亡检测脑缺血再灌注后海马组织bcl-2、Bax表达及凋亡细胞。结果依达拉奉预处理组术后24h原位末端标记（TUNEL）、bcl-2、Bax阳性细胞明显增加，与假手术组比较差异有显著性（P〈0．01）。依达拉奉预处理组术后24hTUNEL、Bax阳性细胞数明显少于对照组（P〈0．01）。依达拉奉预处理组术后24hbcl-2阳性细胞数较对照组明显增加（P〈0．01）。结论凋亡机制参与了脑缺血再灌注后继发性损伤的过程，依达拉奉可能通过上调bcl-2蛋白表达，下调Bax蛋白表达，减轻脑缺血再灌注后的细胞凋亡，增加脑缺血再灌注损伤应激耐受性保护和神经损伤起保护作用。

Effects of Edaravone pretreatment on cells apoptosis and expression of bcl-2, bax, hsp-70 in rats following cerebral ischemia.reperfusion

Objective To observe the effect of edaravone pretreatment on cerebral ischemia-reperfusion neuronal apoptosis and Bcl-2, Bax expression. Methods 45 healthy male SD rats were randomly divided into sham-operated group, saline control group, edaravone pretreatment group of 15 rats. The focal middle cerebral artery occlusion （ MCAO ） model was made by thread-tie method. 12h before MCAO, edaravone pretreatment group were given 3mg/kg, the control group was given normal saline were injected. After 90 rain MCAO following 24 h of reperfusion, the brain of isehemia and reperfusion in hippocampal tissue were used to observe the Bcl-2, Bax expression and apoptosis by immunohistochemical staining and in situ cell death. Results Compared with the sham-operated group, after 24h edaravone pre-treatment group, in situ end labehng （TUNEL）, Bcl-2, Bax- positive cells significantly increased, difference was significant （P 〈 0. 01 ）. Compared with the control group, TUNEL, Bax-positive cells of Edaravone pretreatment group were significantly less than of the control group at the same time point （P 〈 0. 01 ）. Bcl-2 positive cells of Edaravone pretreatment group increased more than that of the control group at the same time significantly （P 〈 0. 01 ）. Conclusions Involved in apoptosis after cerebral ischemia-reperfusion injury secondary to the process of edaravone may be through up-regulating Bcl-2 protein expression and down-regulating Bax protein expression, reducing cerebral ischemia-reperfusion apoptosis to increase the cerebral ischemia-reperfusion injury in stress-tolerance protection and protective effect nerve injury.