安心颗粒对心力衰竭大鼠JAK1-STAT3信号通路的影响

目的：研究安心颗粒对心力衰竭大鼠JAK1-STAT3的影响及其相关机制。方法：将60只SD大鼠随机均分6组各10只：A：空白对照组,B：模型对照组,C：卡托普利组,D：安心颗粒小剂量组,E：安心颗粒中剂量组,F：安心颗粒大剂量组。采用阿霉素腹腔注射法制备心力衰竭大鼠模型,造模同时C、D、E、F组给予药物灌胃。6周后,测定大鼠心功能和心肌肥厚指标、血清白细胞介素-1β（IL-1β）、内皮素（ET）、一氧化氮（NO）、一氧化氮合酶（NOS）水平及心肌糖蛋白130（gp130）、蛋白激酶（JAK1）、信号转导子（STAT3）蛋白表达。结果：模型组IL-1β、NO、NOS、ET浓度及心肌gp130、JAK1、STAT3蛋白表达活性均高于空白对照组（P〈0.05,P〈0.01）,各用药组IL-1β、NO、NOS（D、F组除外）、ET浓度及心肌gp130、JAK1（D、E组除外）、STAT3蛋白表达活性均低于模型组（P〈0.05,P〈0.01）。结论：安心颗粒可抑制细胞因子,减少gp130、JAK1、STAT3蛋白表达,阻断JAK1-STAT3信号传导通路,抑制心肌重塑,改善心肌舒缩功能。

Effect of Anxin Granule on JAK1-STAT3 Signaling Pathway in Rats with Chronic Heart Failure

Objective：To study the effect of Anxin Granule（AXG） on JAK1-STAT3 signaling pathway in rats with chronic heart failure（CHF） and to explore the relative mechanism.Methods：Sixty SD rats were randomly divided into 6 groups：namely normal control group（A）,model group（B）,captopril group（C）,low-dosage AXG group（D）,middle-dosage AXG group（E） and high-dosage AXG group（F）.CHF rat models were established by intraperitoneal injection of small-dose adriamycin.Meanwhile,groups C,D,E and F were received gastric gavage of corresponding drugs respectively.After modeling for 6 weeks,heart function and myocardial hypertrophy index were evaluated,serum IL-1β concentration was examined by enzyme-labeled immunosorbent assay（ELISA）,NO and NOS were detected by721 spectrophotometer for chemical assay,endothelin（ET） was examined by radioimmunoassay,and protein expression of myocardial gp130,JAK1 and STAT3 were tested by western blot assay in each group.Results：Serum IL-1β,NO,NOS and ET concentrations as well as protein expression of gp130,JAK1 and STAT3 were increased in group B（P 0.05 or P 0.01,compared with group A）.Serum IL-1β,NO and NOS concentrations in groups C and E,ET and expression of gp130 and JAK1 in groups C and F,and STAT3 expression in the medication groups were decreased（P 0.05 or P 0.01 compared with those in group B）.Conclusion：AXG can block the JAK1-STAT3 signaling pathway,restrain myocardial remodeling,improve myocardial diastolic and systolic function by inhibiting cell factors and by reducing protein expression of gp130,JAK1 and STAT3.