中文摘要：

目的：研究雷公藤甲素对大鼠心肌H9c2细胞肥大的抑制作用。方法：以0．1、0．3、1．0、3．0、10．0、30．0μg/L雷公藤甲素作用细胞24h，采用MTT法检测细胞活力以筛选最适质量浓度。采用血管紧张素Ⅱ（1．0μmol／L）培养细胞24h以复制细胞肥大模型。实验分为正常对照（常规培养液）组、模型（常规培养液）组与雷公藤甲素①、②、③、④（O．3、1．0、3．0、10．0μg，L）组，复制模型的同时给予相应药物培养24h。染色后荧光镜下观察细胞，以ImageJ软件检测细胞面积；二辛可酸（BCA）法检测细胞蛋白质量浓度；采用实时荧光定量聚合酶链反应（RT-PCR）法检测声．肌球蛋白重链（β-MHC）、心房利钠肽（ANP）和细胞周期蛋白依赖性激酶抑制因子la（CDKNla）mRNA的表达水平。结果：O．1～10μ/L雷公藤甲素对H9c2细胞生长无明显影响。与正常对照组比较，模型组细胞面积、蛋白质量浓度增加，β-MHC、ANP、CDKNla mRNA表达增强，差异有统计学意义（P〈O．01）；与模型组比较，雷公藤甲素②、③、④组细胞面积、蛋白质量浓度减少，β-MHC、ANP、CDKNla mRNA表达减弱，差异有统计学意义（P〈O．01）。结论：雷公藤甲素能抑制大鼠H9c2细胞的肥大反应，其机制可能与下调cDKNla mRNA表达有关。

英文摘要：

OBJECTIVE： To investigate the inhibitory effect of triptolide on rat myocardial H9c2 cell hypertrophy. METHODS： Cells were treated with triptolide （0.1, 0.3, 1.0, 3.0, 10.0, 30.0 gg/L） for 24 h, the cell vitality was detected by MTT to choose the optimal mass concentration. Cells were treated with angiotensin II （1.0μmol/L） for 24 h to generate the cell hypertrophy mod- el. Experiments were divided into normal control group （conventional culture）, model group （conventional culture） and triptolide ①, ②, ③, ④（0.3, 1.0, 3.0, 10.0 μg/L）groups. The cell hypertrophy model were generated and treated with the corresponding drug for 24 h. The cells were observed by using fluorescence microscope after staining; cell areas were determined by Image J; cell protein mass contents were detected by BCA; the mRNA expression levels of β-myosin heavy chain （β-MHC）, atrial natriuretic peptide （ANP） and cylin-dependent kinase inhibitor la （CDKNla） were determined by real-time fluorescent quantitative poly- merase chain reaction （RT-PCR）. RESULTS： 0.1-10 μg/L TP had no obvious effect on H9c2 cell growth. Compared with normal control group, the cell areas and protein mass contents were increased in model group, the mRNA expression of β-MHC, ANP, CDKNla were enhanced, there was statistical significant difference （P〈0.01）. Compared with model group, the cell areas and pro- tein mass contents were decrease in triptolide ②,③,④ groups, the mRNA expression of β-MHC, ANP, CDKNla were de- creased, there was statistical significant difference （P〈0.01）. CONCLUSIONS： Triptolide can inhibit the hypertrophy reaction of rat H9c2, and its mechanism may be related to down-regulation of CDKNla mRNA expression.