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目的:观察醛固酮对主动脉Bcl-2表达的影响。方法:32只SD大鼠随机均分为4组:①空白溶剂设为对照(60%丙二醇+10%乙醇+30%双蒸水);②醛固酮腺瘤:泵入醛固酮(1μg/h);③醛固酮腺瘤+依普利酮组:依普利酮(100mg·kg~(-1)·d~(-1));④醛固酮腺瘤+肼苯哒嗪组:肼苯哒嗪(25 mg·kg~(-1)·d~(-1))。渗透泵内分别注入醛固酮或空白溶剂,然后将其埋植于大鼠背部皮下。8周后,免疫组织化学和免疫印迹检测主动脉Bcl-2的表达。结果:与对照组相比,腺瘤组大鼠主动脉Bcl-2表达显著减少(P<0.05);依普利酮能够拮抗醛固酮对Bcl-2表达的抑制作用(P<0.05)。结论:醛固酮通过抑制Bcl-2表达,调节细胞凋亡状态,可能是醛固酮诱导主动脉重构的机制之一。
Objective: To observe the effect of aldosterone on the expression of Bcl-2 in the aorta. Methods: 32 SD rats were randomly divided into 4 groups: ① blank control group (60% propylene glycol + 10% ethanol + 30% double distilled water); ② aldosterone adenoma: parenteral aldosterone (1 μg / h) (3) Aldosterone adenoma + Eplerenone group: Eplerenone (100 mg · kg -1 · d -1); ④ Aldosterone adenoma + Hydralazine group: Hydralazine (25 mg · kg -1 · d -1). Osmotic pump were injected aldosterone or blank solvent, and then implanted in the back of the rat subcutaneous. After 8 weeks, the expression of Bcl-2 in the aorta was detected by immunohistochemistry and Western blotting. Results: Compared with the control group, the expression of Bcl-2 in the aorta of rats in the adenoma group was significantly decreased (P <0.05). Eplerenone could inhibit the inhibitory effect of aldosterone on the Bcl-2 expression in the adenoma group (P <0.05). Conclusion: Aldosterone may be one of the mechanisms of aldosterone-induced aortic remodeling by inhibiting Bcl-2 expression and regulating apoptosis status.