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c-Jun抑制剂对大鼠心肌纤维化抑制作用

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摘要:

目的 探讨c-Jun抑制剂对盐酸异丙肾上腺素(ISO)所致大鼠心肌纤维化的影响。方法 将 SD雄性大鼠(200±20 g)32只随机等分为对照组、二甲基亚砜(DMSO)组、ISO [5 mg/(kg·d)] 组 (模型组)、ISO [5 mg/(kg·d)]+SP600125[10 mg/(kg·d)] 组(抑制剂组)。各组1次/d给予相关试 剂,连续给药至第7 d时处死大鼠。放射免疫法检测大鼠心房肌组织中血管紧张素Ⅱ(AngⅡ)含量; 常规H-E染色观察心肌纤维化情况;Masson染色法计算胶原容积分数(CVF)并作为心肌纤维化程度的 量化指标;采用免疫组化SP法测定磷酸化c-Jun氨基末端激酶1/2/3(p-JNK1/2/3)、磷酸化c-Jun(p-c- Jun)蛋白的表达。结果 AngⅡ在模型组和抑制剂组中含量较对照组、DMSO组显著升高且差异有统计学 意义(P均<0.01);模型组与对照组、DMSO组、抑制剂组相比出现明显的心房纤维化(P均<0.01)且 心肌组织中p-JNK1/2/3和p-c-Jun的含量较高,差异有统计学意义(P均<0.01),抑制剂组与对照组和 DMSO组相比心肌纤维化程度及心肌组织中p-JNK1/2/3和c-Jun的含量差异无统计学意义(P均>0.05)。 结论 c-Jun抑制剂可减轻ISO诱发的大鼠心肌纤维化,其机制可能与抑制JNK信号转导通路有关。

Abstract:

Objective To discuss the influence of inhibitor of c-Jun on myocardial fibrosis induced by isoprenaline (ISO) in rats. Methods Male SD rats (n=32, weight=200±20g) were randomly divided into control group, DMSO group, ISO group [5 mg/(kg·d), model group] and ISO+SP600125 group [5 mg/(kg·d)+10 mg/ (kg·d), inhibitor group]. Each group was given corresponding drugs once a day and after continuous medication for 7 d, all rats were executed. The content of angiotensin Ⅱ (Ang Ⅱ) in atrial muscle tissue was detected by using radioimmunoassay (RIA). The status of myocardial fibrosis was observed after routine H-E staining, and collagen volume fraction (CVF) was calculated by using Masson staining, which was taken as a quantitative index for severity of myocardial fibrosis. The expressions of phosphorylated c-Jun N-terminal kinase 1/2/3 (p-JNK1/2/3) and phosphorylated c-Jun (p-c-Jun) protein were detected by using immunohistochemical SP method. Results The content of AngⅡ increased significantly in model group and inhibitor group compared with control group and DMSO group (all P<0.01). There was significant myocardial fibrosis observed, and content of p-JNK1/2/3 and p-c- Jun were higher in model group compared with control group, DMSO group and inhibitor group (all P<0.01). The difference in severity of myocardial fibrosis and content of p-JNK1/2/3 and p-c-Jun had no statistical significance among inhibitor group, control group and DMSO group (all P>0.01). Conclusion The inhibitor of c-Jun can relieve the myocardial fibrosis induced by ISO, and the mechanism may be related to inhibition of JNK signaling pathway.

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  • 2008

  • 1

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