毛蕊异黄酮抑制压力超负荷大鼠心肌肥厚及对JAK/STAT信号通路的影响  

The potential protect effect and mechanism of calycosin on cardiac hypertrophy in rats

作　　者：黄璟[1] 成传访[1] 李惠波 罗燕华[2] 区文超[1] HUANG Jing;CHENG Chuanfang;LI Huibo;LUO Yanhua;OU Wenchao(Department of Cardiology,the Second Affiliated Hospital of Guangzhou Medical University/Guangzhou Institute of Cardiovascular Disease,Guangzhou 510260,China)

机构地区：[1]广州医科大学附属第二医院心内科(广州心血管疾病研究所),广州510260 [2]广州医科大学附属第二医院超声科,广州510260

出　　处：《实用医学杂志》2018年第24期4060-4063,共4页The Journal of Practical Medicine

基　　金：广东省中医药局科研资助项目(编号:20151287)

摘　　要：目的探讨毛蕊异黄酮对大鼠心肌肥厚的保护作用及潜在机制。方法使用腹主动脉缩窄(TAAC)制备大鼠心肌肥厚模型,将SD大鼠随机分为TAAC组、溶剂对照组(vehicle组)以及毛蕊异黄酮处理组(calycosin组),术后1周每天腹腔给药。8周后行超声心动图检查,检测左心室有创压以及心脏组织中JAK1、STAT3蛋白表达量。结果 8周后,与TAAC组、vehicle组相比较,calycosin组大鼠左心室质量指数(LVMI)、IVS、LVESD、LVESV均明显降低(P <0.05),LVEDD、LVEDV明显升高(P <0.05),LVEF无明显改变(P> 0.05);calycosin组大鼠心室收缩末压及±dp/dt明显升高(P <0.05);calycosin组心肌组织JAK1、STAT3蛋白表达量明显下降,差异有统计学意义(P <0.05)。而TAAC组与vehicle组比较差异无统计学意义(P> 0.05)。结论毛蕊异黄酮在大鼠压力负荷心肌肥厚中起保护作用,其机制可能与抑制JAK/STAT信号通路有关。Objective To investigate the potential protect effect and mechanism of calycosin on cardiac hypertrophy in rats.Methods The rat cardiac hypertrophy models were produced by transverse abdominal aortic constriction(TAAC). SD rats were randomly divided into TAAC group,vehicle group and calycosin group. Rats in these three group received the corresponding drugs by intraperitoneal injection once a day at one week after surgery.Echocardiogram examination was performed at eight weeks after surgery,the invasive pressure of left ventricle and protein expression levels of JAK1/STAT3 in myocardial tissue were also detected.Results At 8 weeks after sur-gery,comparison with TAAC and vehicle group,LVMI,IVS,LVESD and LVESV were significantly decreased in calycosin group(P < 0.05),with no significant difference in LVEF in three group(P > 0.05). Comparison with TAAC and vehicle group,the diastolic pressure,+dp/dtmax and-dp/dtmax were significantly increased in calyco-sin group(P < 0.05,respectively),and protein expression of JAK1 and STAT3 was significantly declined in caly-cosin group(P < 0.05).Conclusions Calycosin plays a protective effect in rat cardiac hypertrophy induced by pressure overload via inhibiting JAK/STAT signal pathway.

关 键 词：毛蕊异黄酮 心肌肥厚 JAK/STAT信号通路 

分 类 号：R285.5[医药卫生—中药学]