摘要
目的探讨氟伐他汀对糖尿病大鼠心肌间质纤维化以及心脏结构和功能的影响。方法雄性SD大鼠24只随机分为3组:正常对照组、模型组、氟伐他汀组,均n=8。采用链脲佐菌素一次性腹腔注射建立糖尿病动物模型,12 wk后检测大鼠血流动力学和生化指标,RT-PCR法分析左室心肌结缔组织生长因子(CTGF)mRNA表达,Western blotting观察CTGF蛋白质表达,天狼猩红染色测量心肌组织胶原含量。结果与正常对照组相比,糖尿病大鼠左心室收缩压峰值(LVSP)、左心室压最大上升和下降速度(±dp/dtmax)均显著减低(P<0.01),左心室舒张末期压(LVEDP)、CTGF mRNA和蛋白表达水平、左室心肌组织胶原含量均显著升高(P<0.05或P<0.01);应用氟伐他汀干预治疗后,与模型组相比,LVSP、±dp/dtmax显著升高(P<0.05),LVEDP、CTGF mRNA和蛋白表达水平及胶原含量均显著降低(P<0.05)。结论氟伐他汀可逆转糖尿病大鼠心肌间质纤维化并改善心功能,这种作用可能与其抑制CTGF的表达有关。
AIM To investigate the effects of fluvastatin on myocardial interstitial fibrosis and cardiac function in diabetic rats.METHODS Twenty-four male SD rats were randomly divided into control group,model group,and fluvastatin group（n = 8 for each）.Diabetes was induced after a single intraperitoneal injection of streptozotocin.After 12 weeks intervention,the hemodynamic and serum biochemical parameters were measured in the rats.Then myocardium tissues were collected,the expression of CTGF mRNA and protein and collagen content were detected.RESULTS Compared with the control group,the left ventricular systolic pressure（LVSP）and ±dp/dtmax were significantly decreased and left ventricular end diastolic pressure（LVEDP）were significantly increased in the model group（P 0.01）.The mRNA and protein expression of CTGF and the collagen content were significant higher in the model group than those in the control group（P 0.05 or P 0.01）.After fluvastatin administration,compared with the model group,LVSP and ±dp/dtmax were increased significantly（P 0.05）;CTGF mRNA and protein expression,LVEDP,and the collagen content were obviously attenuated（P 0.05）.CONCLUSION Fluvastatin could inhibit myocardial interstitial fibrosis and improve the cardiac function of diabetic rats,which might be related to the down-regulating of the CTGF expression.
出处
《中国新药与临床杂志》
CAS
CSCD
北大核心
2010年第11期837-841,共5页
Chinese Journal of New Drugs and Clinical Remedies
关键词
糖尿病
氟伐他汀
心室功能
左
心肌纤维化
结缔组织生长因子
diabetes mellitus fluvastatin ventricular function left myocardial fibrosis connective tissue growth factor
