摘要
目的观察银杏酮酯(GBE50)对急性血瘀证大鼠血流动力学和心肌组织肿瘤坏死因子(TNF)-α通路的影响,探讨其作用机制。方法采用皮下注射盐酸肾上腺素复合冰水浴法制作大鼠急性血瘀证模型。将雄性SD大鼠随机分为正常组、模型组和GBE50组,灌胃相应药物干预11 d后造模。次日观察各组血流动力学变化,RT-PCR检测心肌组织TNF-α、TNFR1、TNFR2 m RNA表达,放免法检测心肌组织TNF-α蛋白表达,免疫组化检测心肌组织TNFR1和TNFR2蛋白表达。结果模型组血流动力学指标呈现低于正常组的趋势;与模型组比较,GBE50组左心室收缩峰压平均值、左室发展压明显增大,室内压最大上升速率时间明显减少(P<0.05),GBE50组心肌组织TNF-α、TNFR1、TNFR2蛋白表达明显升高,TNFR2 m RNA表达明显升高(P<0.05)。结论 GBE50能改善急性血瘀证大鼠血流动力学指标,并对心肌组织TNF-α通路具有调控作用,增加保护性受体TNFR2表达可能是其保护心功能的机制之一。
Objective To observe the effects of Ginkgo biloba extract 50(GBE50) on hemodynamics and myocardial tissue TNF-α pathway in rats with acute blood stasis syndrome; To discuss its mechanism of action. Methods A model of acute blood stasis syndrome was established by subcutaneous injection of epinephrine hydrochloride and ice bath. Male SD rats were divided randomly into normal group, model group and GBE50 group. After medicine was administrated by gavage for 11 days, the acute blood stasis model was established. The hemodynamic changes were observed in the next day. The expressions of TNF-α, TNFR1 and TNFR2 m RNA were detected by RT-PCR. The expressions of TNF-α, TNFR1 and TNFR2 protein were tested by radioimmunoassay and immunohistochemistry. Results The hemodynamics of the model group was lower than that of the normal group. Compared with model group, GBE50 could increase m LVSP, DP and decrease t-dp/dtmax(P0.05). The protein expressions of TNF-α, TNFR1, and TNFR2 in GBE50 group were higher than those in model group, and TNFR2 m RNA expression increased significantly in GBE50 group(P0.05). Conclusion GBE50 can ameliorate the decline of hemodynamics of rats with acute blood stasis syndrome, and regulate the myocardial TNF-α pathway. Increasing the expression of protective receptor TNFR2 may be one of the mechanisms of protecting cardiac function.
出处
《中国中医药信息杂志》
CAS
CSCD
2017年第11期34-38,共5页
Chinese Journal of Information on Traditional Chinese Medicine
基金
国家自然科学基金(81303256)