小檗碱对压力负荷所致心肌肥厚大鼠的保护作用

发布时间：2018-06-20 20:40

本文选题：小檗碱 + 主动脉缩窄　；参考：《南京医科大学学报(自然科学版)》2015年01期

【摘要】：目的:通过动物实验探讨小檗碱(Berberine)对压力负荷所致大鼠心肌肥厚模型的保护作用,并探讨其作用机制。方法:通过主动脉缩窄术构建大鼠心肌肥厚模型,将造模成功的16只SD大鼠随机分为模型组及模型+小檗碱组,另外将假结扎主动脉的8只大鼠入组假手术组。术后4周,利用心脏超声测定大鼠的心功能指标;HE、Masson及TUNEL染色等分子生物学方法测定心肌细胞大小、心脏纤维化、心肌细胞凋亡等指标;同时使用RT-q PCR法检测左室心肌组织心房利钠因子(ANP)m RNA的表达;采用Western blot的方法检测内质网应激相关指标Bip/GRP78和CHOP的蛋白表达情况。结果 :与模型组相比,小檗碱可明显改善主动脉缩窄所致的心功能紊乱,显著降低心肌细胞大小(P0.05)、心脏组织的纤维化程度以及心肌细胞凋亡比率(P0.05);Western blot结果表明,小檗碱治疗可明显降低长期压力超负荷所致的内质网应激相关指标Bip/GRP78和CHOP的表达的增加(P0.05)。结论 :小檗碱可显著改善压力超负荷所致的心肌肥厚及心功能紊乱,抑制心肌细胞凋亡,对肥厚型心肌起保护作用,且此种心脏保护性作用可能与其抑制压力负荷所致的内质网应激相关。
[Abstract]:Aim: to investigate the protective effect of Berberine on myocardial hypertrophy induced by pressure load in rats and its mechanism. Methods: myocardial hypertrophy model was established by coarctation of aorta in rats. Sixteen SD rats were randomly divided into model group and model berberine group, and 8 rats with pseudoligation of aorta were added into sham operation group. At 4 weeks after operation, cardiac function indexes such as myocardial cell size, cardiac fibrosis and cardiomyocyte apoptosis were measured by echocardiography and Tunel staining. RT-PCR was used to detect the expression of atrial natriuretic factor (ANPM) mRNA in left ventricular myocardium, and Western blot was used to detect the protein expression of Bip-GRP78 and chop, which were related to endoplasmic reticulum stress. Results: compared with the model group, berberine could significantly improve the cardiac dysfunction induced by aortic coarctation, decrease the size of cardiac myocytes and decrease the degree of cardiac fibrosis and the ratio of cardiomyocyte apoptosis. The results of Western blot showed that berberine could improve the cardiac function induced by coarctation of aorta and decrease the size of cardiac myocytes. Berberine treatment could significantly reduce the increase of Bip-GRP78 and chop expression in endoplasmic reticulum stress induced by long-term pressure overload. Conclusion: berberine can significantly improve myocardial hypertrophy and cardiac dysfunction induced by pressure overload, inhibit cardiomyocyte apoptosis and protect hypertrophic myocardium. This cardioprotective effect may be related to the inhibition of endoplasmic reticulum stress induced by pressure load.
【作者单位】：南京医科大学附属南京医院心内科;
【基金】：江苏省普通高等学校研究生科研创新项目(2013CXLX11-511)
【分类号】：R96

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