黄芩苷对大鼠缺血再灌注脑组织TNF-α、IL-1β表达的影响

Effects of Baicalin on the expression of TNF-α, IL-1β in cerebral tissue after local cerebral ischemia-reperfusion in rats

目的探讨黄芩苷对大鼠缺血再灌注脑组织TNFα、IL1β的表达和脑水肿及超微结构的影响。方法采用大脑中动脉缺血再灌注模型,先将大鼠随机分为假手术组、缺血再灌注组及黄芩苷治疗组,再用免疫组化法检测脑组织缺血再灌注3、6、24hTNFα和IL1β的表达,用称重法测定缺血再灌注3、6h脑组织含水量,电子显微镜观察缺血再灌注24h脑组织的超微结构及黄芩苷对其影响。结果TNFα和IL1β在缺血再灌注3、6、24h明显表达,黄芩苷治疗组的表达较之明显降低(P<0.01);缺血再灌注3、6h脑组织含水量明显增高,黄芩苷治疗组脑组织含水量较之明显降低(P<0.05,P<0.01);脑组织超微结构显示:神经细胞肿胀、损伤以及细胞迟发性死亡程度显著减轻。结论黄芩苷能降低脑缺血再灌注后TNFα、IL1β的表达,具有一定的脑组织保护作用。

Objective To study the effects of Baicalin on the cerebral edema, expression of TNF-α and IL-1β and ultrastructure in local cerebral ischemia-reperfusion in rats. Methods The rats were randomly divided into sham operated control group, ischemia-reperfusion group and Baicalin treatment group. The local cerebral ischemia-reperfusion models were established by middle cerebral artery occusion(MCAO). The contents of brain water were measured with dry-wet at 3 hour and 6 hour after ischemia-reperfusion. The expression of TNF-α and IL-1β at 3 h, 6 h, 24 h after ischemia-reperfusion and the effects of Baicalin on them were evaluated with immunohistochemical method. The ultrastructure was observed under electron microscope at 24 hour after ischemia-reperfusion. Results The expressions of TNF-α and IL-1β were very low in sham operated control group. At 3 h, 6 h, 24 h after ischemia-reperfusion, the expressions were significantly increased; In the groups treated with Baicalic, the expressions were significantly decreased. The contents of brain water increased more significantly in ischemia-reperfusion group at 3 hour or 6 hour than that in sham operated control group; and compared with ischemia-reperfusion group, the contents of brain water in Baicalin treatment group were decreased significantly (P<0.05～0.01). Compared with ischemia-reperfusion group, the degrees of edema, impairment and death of nerve cells were lightened in Baicalin treatment group at 24 hour after ischemia-reperfusion. Conclusion Baicalin may decrease the expressions of TNF-α and IL-1β, and has a protective effect on the cerebral ischemia tissue during the ischemia-reperfusion.