补阳还五汤对MCAO大鼠不同时间点脑组织病理形态及NO、vWF、6-keto-PGF1α表达的影响

Effects of Buyang Huanwu Decoction on brain tissue pathologic morphology and expression of NO, vWF and 6-keto-PGF1α in rat model of MCAO at different time points

目的:探讨补阳还五汤对中脑动脉闭塞(MCAO)后局灶性脑缺血大鼠不同时间点脑组织病理形态及一氧化氮(NO)、血管性假血友病因子(v WF)、6-酮-前列腺素F1α(6-keto-PGF1α)表达的影响。方法:用颈内动脉线栓法建立MCAO模型,采用HE染色、TUNEL法观察缺血后1d、3d、7d脑组织病理形态;采用酶联免疫吸附法(ELISA)测定血浆中NO、v WF、6-keto-PGF1α的表达。结果:与模型组同期比较,补阳还五汤组脑组织梗死范围在治疗后7d减少最明显(P<0.01),细胞凋亡率治疗后7d降低最明显(P<0.01);脑缺血后7d,依达拉奉组和补阳还五汤组血浆NO表达水平均较模型组同期明显升高(P<0.01),补阳还五汤组在治疗后7d NO升高最明显(P<0.01);脑缺血后3、7d,依达拉奉组和补阳还五汤组血浆v WF表达水平较模型组同期明显降低(P<0.01),补阳还五汤组在治疗后3d v WF降低最明显(P<0.01),与模型组同期比较,补阳还五汤组治疗后7d6-keto-PGF1α水平显著增加(P<0.01)。结论:补阳还五汤能通过减少脑组织梗死范围、降低细胞凋亡率,下调v WF、上调NO、6-keto-PGF1α水平表达,从而有效保护脑组织。

Objective： To explore the effects of Buyang Huanwu Decoction（BHD） on brain tissue pathologic morphology and expression of nitric oxide（NO）, von willebrand factor（v WF） and 6-keto prostaglandin 1α（6-keto-PGF1α） in rat model of MCAO at different time points. Methods： The rat model of MCAO was established by the method of nylon monofilament via the internal carotid artery. The pathologic morphology of brain tissues after ischemia in day 1, day 3 and day 7 were observed by hematoxylin-eosinstaining（HE） and transferase-mediated deoxyuridine triphosphate-biotin nick end labeling（TUNEL） method. The levels of NO, v WF and 6-keto-PGF1α in plasma were detected by ELISA. Results： The treatment of BHD significantly reduced the cerebral infarction scope after the treatment for 7 days when compared with the model group（P〈0.01）, and BHD significantly decreased the cell apoptosis rate after the treatment for 3 days（P〈0.01）. The level of NO was significantly increased in the sham operation group, daravone group and BHD group after the ischemia for 7 days when compared with the model group（P〈0.01）, and the BHD group showed the most obvious effect. The level of v WF was significantly decreased in the daravone group and BHD group after the ischemia for 3 and 7 days when compared with the model group（P〈0.01）, and the BHD group showed the most obvious effect when treating for 3 days. In addition, on the 7th day after treatment, the level of 6-keto-PGF1αin the BHD group significantly increased compared with the model group at the same time point（P〈0.01）. Conclusion： BHD can protect brain tissue of MCAO rat by decreasing the cerebral infarction scope and the cell apoptosis rate, down-regulating the level of v WF and up-regulating the levels of NO and 6-keto-PGF1α.