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目的探讨西格列汀对阿霉素诱导的慢性充血性心力衰竭的保护效应及机制。方法 SD大鼠随机分为4组:空白对照组(NC组),ADR模型组、JAN+ADR组、JAN组;JAN+ADR组与JAN组分别给予西格列汀40 mg/(kg·d)灌胃持续6周(首剂加倍),ADR模型组和ADR+JAN组腹腔注射阿霉素4 mg/(kg·周),持续6周;NC组灌胃等量生理盐水。称量大鼠重量和心脏重量,计算心脏指数;使用Masson染色观察心肌细胞胶原纤维分布情况;使用免疫组织化学方法检测凋亡相关蛋白Caspase-3和BAX蛋白的表达。结果 ADR组心脏体重指数与NC组相比明显增加(P<0.05),JAN+ADR组和JAN组心脏体重指数与NC组相比无明显差异;ADR组的心肌胶原成分明显较其他各组多,心肌细胞体积增大,组织结构排列紊乱,而JAN+ADR组与NC组相比没有明显差异;JAN组能够抑制阿霉素引起的心肌细胞凋亡相关蛋白Caspase-3和Bax蛋白的表达。结论西格列汀可以抑制阿霉素诱导的慢性充血性心力衰竭,其机制可能与抑制心肌细胞凋亡和纤维化有关。
Objective To investigate the protective effect and mechanism of sitagliptin on doxorubicin-induced chronic congestive heart failure. Methods SD rats were randomly divided into 4 groups: control group (NC group), ADR model group, JAN + ADR group, JAN group; JAN + ADR group and JAN group were given sitagliptin 40 mg / (kg · d ) For 6 weeks (the first dose was doubled). ADR model group and ADR + JAN group were given adriamycin 4 mg / (kg · d) intraperitoneally for 6 weeks. The rats in NC group were given the same amount of normal saline. The weight of rat and heart weight were measured to calculate the cardiac index. The distribution of collagen fibers in cardiomyocytes was observed by Masson staining. The expressions of Caspase-3 and BAX protein were detected by immunohistochemistry. Results The body mass index of ADR group was significantly higher than that of NC group (P <0.05). There was no significant difference between JAN + ADR group and JAN group in cardiac mass index and NC group. The content of myocardial collagen in ADR group was significantly higher than that in NC group , The volume of cardiomyocytes increased, the arrangement of tissues was disorganized, while there was no significant difference between JAN + ADR group and NC group; JAN group could inhibit the expression of Caspase-3 and Bax protein induced by doxorubicin. Conclusion Sitagliptin can inhibit doxorubicin-induced chronic congestive heart failure, the mechanism may be related to the inhibition of myocardial apoptosis and fibrosis.