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目的探讨辛伐他汀对大鼠心肌梗死后心室重构和FoxO3a表达的影响。方法建立大鼠MI模型,24 h后存活大鼠随机分成心肌梗死组(MI组,n=8)、辛伐他汀20 mg组[20 mg/(kg.d),Sim组,n=8],并同时建立假手术组(Sham组,n=10)。4周后观察心室质量指数(LVWI)、天狼猩红染色分析左室非梗死区胶原容积分数(CVF)、HE染色观察心肌组织病理改变,RT-PCR和Western blot检测FoxO3a在非梗死区mRNA和蛋白表达水平。结果 MI组较Sham组LVWI[(2.62±0.16)vs(1.80±0.13),P<0.05]、非梗死区Ⅰ型胶原容积分数[(18.81±2.65)vs(5.01±0.84),P<0.05]、Ⅲ型胶原容积分数[(3.83±0.38)vs(1.52±0.23),P<0.05]及Ⅰ/Ⅲ比值[(4.96±0.90)vs(3.31±0.40),P<0.05]显著增加;左室心肌非梗死区FoxO3a mRNA[(0.29±0.05)vs(0.57±0.06),P<0.05]与蛋白[(0.28±0.04)vs(0.62±0.07),P<0.05]表达均降低。与MI组相比,Sim组LVWI[(2.27±0.08)vs(2.62±0.16),P<0.05]、非梗死区I型胶原容积分数[(9.26±1.13)vs(18.81±2.65),P<0.05]、Ⅲ型胶原容积分数[(2.37±0.23)vs(3.83±0.38),P<0.05]及Ⅰ/Ⅲ比值[(3.98±0.79)vs(4.96±0.90),P<0.05]均显著下降;但高于Sham组(P<0.05);左室心肌非梗死区FoxO3a mRNA[(0.49±0.06)vs(0.29±0.05),P<0.05]与蛋白[(0.38±0.08)vs(0.28±0.04),P<0.05]表达均显著增高;但低于Sham组(P<0.05),心肌组织病理结构得到改善。结论辛伐他汀能有效改善MI后心肌损伤和心室重构,其机制可能与其在基因转录和蛋白质翻译水平促进FoxO3a表达综合作用有关。
Objective To investigate the effect of simvastatin on ventricular remodeling and FoxO3a expression after myocardial infarction in rats. Methods MI rats were randomly divided into myocardial infarction group (MI group, n = 8), simvastatin 20 mg group (20 mg / (kg · d), Sim group, n = 8) , And sham-operated group was also established (Sham group, n = 10). After 4 weeks, the ventricular mass index (LVWI) was observed. The ventricular non-infarction volume fraction (CVF) was analyzed by Sirius red staining. The pathological changes of myocardium were observed by HE staining. Protein expression levels. Results LVWI was significantly higher in MI group than in Sham group [(2.62 ± 0.16) vs (1.80 ± 0.13), P <0.05], but not in infarct area [(18.81 ± 2.65 vs 5.01 ± 0.84, P <0.05] (P <0.05), and the volume fraction of type Ⅲ collagen [(3.83 ± 0.38) vs (1.52 ± 0.23), P <0.05] and Ⅰ / Ⅲ ratio [(4.96 ± 0.90) vs (3.31 ± 0.40) Compared with the protein [(0.28 ± 0.04) vs (0.62 ± 0.07), P <0.05], the expression of FoxO3a mRNA in non-infarcted myocardium was significantly lower than that in control group [(0.29 ± 0.05 vs 0.57 ± 0.06, P <0.05; Compared with MI group, the LVWI in Sim group was (2.27 ± 0.08) vs (2.62 ± 0.16), P <0.05, and that in non-infarct zone was 9.26 ± 1.13 vs 18.81 ± 2.65, P < 0.05], P <0.05], the ratio of type Ⅲ collagen [(2.37 ± 0.23) vs (3.83 ± 0.38), P <0.05] and Ⅰ / Ⅲ ratio [(3.98 ± 0.79) vs (4.96 ± 0.90) (0.49 ± 0.06) vs (0.29 ± 0.05), P <0.05] and protein [(0.38 ± 0.08) vs (0.28 ± 0.04 ), P <0.05], but lower than that in Sham group (P <0.05). The pathological structure of myocardial tissue was improved. Conclusion Simvastatin can improve myocardial injury and ventricular remodeling after MI. The mechanism may be related to its role in promoting FoxO3a expression in gene transcription and protein translation.