脱氧皮质酮诱导大鼠心肌细胞凋亡及阿利吉仑干预的影响
| 作者: |
1华锦胜,
1许邦龙
1 安徽医科大学第二附属医院心血管内科，合肥 230601 |
| 通讯: |
华锦胜
Email: www.huajs@qq.com |
| DOI: | 10.3978/j.issn.2095-6959.2015.03.012 |
摘要
目的：探讨阿利吉仑对脱氧皮质酮诱导的大鼠心肌凋亡的影响及其相关机制。方法：将45只SD大 鼠行右肾切除，术后予1%氯化钠饮水4周并随机分为3组：对照(A)组、脱氧皮质酮(B)组、脱氧皮 质酮+阿利吉仑(C)组。大鼠心脏组织经TUNLE染色法测定心肌细胞的凋亡表达，免疫组化法观察 Bax、Bcl-2及单核巨噬细胞抗原(ED-1)的表达。酶联免疫(enzyme-linkecl immunoabsorbent assay， ELISA)法检测大鼠血浆中脑钠肽(brain natriuretic peptide，BNP)的水平。结果：与A比较，B组的凋 亡指数(apoptosis index，AI)、心肌Bax的表达、血管周围的巨噬细胞浸润及血浆BNP水平明显增加 (P<0.01)，而Bcl-2的表达则明显减少(P<0.01)；较B组相比，C组AI、心肌Bax的表达、血管周围的 巨噬细胞浸润及血浆BNP水平明显降低(P<0.01)，而Bcl-2的表达则明显升高(P<0.01)。结论：阿利 吉仑能减少心肌细胞的炎性细胞浸润、调节Bcl-2/Bax的表达，显著减少心肌凋亡、改善心功能。
关键词：
阿利吉仑
脱氧皮质酮
心肌凋亡
慢性心衰
Effect of aliskiren on desoxycorticosterone acetate-salt induced cardiomyocyte apoptosis in rats
CorrespondingAuthor: HUA Jinsheng Email: www.huajs@qq.com
DOI: 10.3978/j.issn.2095-6959.2015.03.012
Abstract
Objective: To investigate the effects and mechanisms of aliskiren on desoxycorticosterone acetate-salt induced cardiomyocyte apoptosis in rats. Methods: A total of 45 male SD rats underwent right nephrectomy and bred with 1% sodium chloride for 4 weeks. Then, these rats were randomly divided into 3 groups: 1) A group: animals were subcutaneously implanted with Silicone rubber and intragastrically treated with 1% sodium chloride once daily; 2) B group: animals were subcutaneously implanted with silicone rubber impregnated with DOCA (200 mg per rat) and intragastrically treated with 1% sodium chloride once daily; 3) animals were subcutaneously implanted with silicone rubber impregnated with DOCA (200 mg per rat) and intragastrically treated with aliskiren at 50 mg/kg·d-1 once daily. TUNEL was done to observe cardiomyocyte apoptosis, immunohistochemistry was employed to detect the protein expressions of Bax, Bcl-2 and ED-1. Enzyme-linked immunoabsorbent assay (ELISA) was performed to determine brain natriuretic peptid. Results: The myocardial inflammation and cardiomyocyte apoptosis was observed in B group. Compared with the other groups, the index of apoptosis and expression of ED-1 were increased markedly (P<0.01). Compared with B group, brain natriuretic peptide (BNP) in plasma and expression of Bax were significantly decreased in C group (P<0.01). But the level of Bcl-2 was just the opposite (P<0.01). Conclusion: These results suggest that aliskiren may attenuate desoxycorticosterone acetate-salt induced cardiomyocyte apoptosis in rats. Macrophage infiltration may be responsible for the effects.