摘要
目的:观察表没食子儿茶素没食子酸酯(EGCG)对野百合碱(MCT)所致大鼠右心室肥厚的影响并探讨其可能的机制。方法:40只雄性SD大鼠随机分为正常组,模型组,EGCG(40 mg·kg-1)组和阳性药卡托普利(25 mg·kg-1)组,每组10只。除正常组外,采用野百合碱诱导制备右心肥厚大鼠模型,24 h后各组分别ig给药,正常组和模型组ig等体积生理盐水,每天1次,连续21 d,观察EGCG对模型大鼠右室肥厚指数(RVHI),右心室质量指数(RVMI),右心室心肌细胞超微结构的变化的影响;对右室心肌组织一氧化氮(NO),诱导性一氧化氮合酶(i NOS),白细胞介素-1β(IL-1β)及IL-6含量的影响。结果:与正常组比较,模型组RVHI,RVMI明显增高(P<0.05),其右心室组织NO,i NOS,IL-1β及IL-6水平明显升高(P<0.05);与模型组比较,EGCG(40 mg·kg-1)组RVHI,RVMI明显降低(P<0.05),右室心肌组织的NO,i NOS,IL-1β及IL-6水平明显降低(P<0.05)。结论:EGCG能有效抑制MCT诱导的大鼠右心室肥厚,其作用途径与其降低右心室心肌组织i NOS表达和NO过多产生及降低IL-1β及IL-6水平有关。
Objective: To observe the effects of epigallocatechin gallate( EGCG) on right ventricular hypertrophy induced by monocrotaline( MCT) in rats and explore its mechanisms. Method: Forty male Wistar rats were randomly divided into the normal group,the model group,the captopril group( 25 mg·kg- 1) and the EGCG( 40 mg·kg- 1) group. MCT-induced right ventricular hypertrophy model in rats was established,and the effects on right ventricular hypertrophy index( RVHI),right ventricular myocardial infarction( RVMI),nitric oxide( NO),inducible nitric oxide synthase( i NOS),interleukin-1β( IL-1β) and IL-6 of right ventricular hypertrophy myocardium tissue and right ventricular myocardial cells in rats were examined. Result: Compared with the normal group,RVHI and RVMI were significantly elevated( P〈0. 05),and NO,i NOS,IL-6 and IL-1βlevel of right ventricular hypertrophy myocardium tissue increased( P〈0. 05) in the model group. Compared with the model group,RVHI and RVMI was obviously declined( P〈0. 05),while levels of NO,i NOS,IL-6 and IL-1βsignificantly decreased( P〈0. 05) in the EGCG group. Conclusion: EGCG could significantly inhibit the RVH induced by MCT in rats. Its mechanisms may be related to reducing the levels of i NOS,NO,IL-1β and IL-6 in right ventricular hypertrophy myocardium tissue.
出处
《中国实验方剂学杂志》
CAS
CSCD
北大核心
2015年第13期126-129,共4页
Chinese Journal of Experimental Traditional Medical Formulae
基金
重庆市卫生局医学科研项目(2012-1-096)
重庆市高等教育教学改革研究重点项目(132128
133309)
万州区科技计划项目(201203055)