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目的:考察心衰Ⅰ号联合贝那普利对慢性心力衰竭(CHF)大鼠心功能和糖调节蛋白78(GRP78)、CCAAT增强子结合蛋白同源蛋白(CHOP)及X盒结合蛋白(XBP1)的影响。方法:将CHF模型大鼠分5组:模型组、心衰Ⅰ号组、贝那普利组、心衰I号+贝那普利组(联合组),并设假手术组,各组连续给药28 d。记录大鼠体征、死亡、心功能情况,测定心肌组织CHOP、GRP78、XBP1表达,血清丙二醛(MDA)和超氧化物歧化酶(SOD)水平。结果:无死亡大鼠。与假手术组比较,模型组大鼠SBP、DBP、CO、LVSP、±dp/dtmax及血清SOD显著降低(P<0.05),心肺指数、LVEDP、血清MDA水平及心脏CHOP、GRP78、XBP1蛋白表达显著升高(P<0.05)。各给药组上述指标不同程度改善,以联合用药组效果最佳(P<0.05)。结论:心衰Ⅰ号联合贝那普利可改善CHF大鼠的心功能,降低心肌CHOP、GRP78及XBP1蛋白表达,降低血清MDA含量并升高SOD活性,提示心衰Ⅰ号通过抑制ERS介导的信号通路达到抑制心肌细胞凋亡的目的。
Objective: To investigate the effects of heart failure Ⅰ combined with benazepril on heart function and the expression of carbohydrate regulatory protein 78 (GRP78), CCAAT enhancer binding protein homologous protein (CHOP) and X box binding protein (XBP1) in chronic heart failure (CHF) )Impact. Methods: CHF model rats were divided into 5 groups: model group, heart failure Ⅰ group, benazepril group, heart failure I + benazepril group (combined group), and sham operation group, each group continuous Dose 28 d. The signs, death and cardiac function of rats were recorded. The expression of CHOP, GRP78 and XBP1 in myocardium were measured, and the levels of serum malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. Results: No dead rats. Compared with sham group, SBP, DBP, CO, LVSP, ± dp / dtmax and serum SOD in model group were significantly lower than those in sham operation group (P <0.05). Cardiorespiratory index, LVEDP, MDA level in serum and CHOP, GRP78 and XBP1 Significantly increased (P <0.05). The above-mentioned indexes in each administration group improved to different degrees, and the combined administration group had the best effect (P <0.05). CONCLUSION: Heart failure Ⅰ combined with benazepril can improve heart function, decrease the expression of CHOP, GRP78 and XBP1 in myocardium, decrease the content of serum MDA and increase the activity of SOD, suggesting that heart failure Ⅰ inhibits ERS-mediated Of the signal pathway to achieve the purpose of inhibiting cardiomyocyte apoptosis.