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目的:探讨阿托伐他汀对慢性心力衰竭过程中Fas/FasL系统影响及联合辅酶Q10的作用。方法:采用阿霉素腹腔注射法复制大鼠心力衰竭模型(2.5 mg/kg,每周给药3次,给药2周),将30只Wistar大鼠分为空白组(6只)及心衰模型组(24只),给药完毕后观察2周,将心衰模型组大鼠随机均分为心衰组、阿托伐他汀治疗组[3.75 mg/(kg.d)]、辅酶Q10治疗组[2.8 mg/(kg.d)]、联合治疗组,连续灌胃2个月。超声检测大鼠心功能,免疫组化法检测心肌组织中Fas、FasL蛋白水平,并观察大鼠心肌细胞凋亡情况。结果:相较于空白组,其余各组均有不同程度的心功能减低,心肌细胞凋亡、Fas与FasL蛋白阳性表达增加,以心衰组最明显。相较于心衰组,3个治疗组凋亡细胞数目、Fas与FasL蛋白阳性表达细胞均降低,联合治疗组较单药治疗组进一步降低。结论:心衰大鼠心肌组织Fas、FasL蛋白表达、细胞凋亡均增加,Fas/FasL系统在心脏由代偿性心肌肥厚向心衰转变过程中起到重要作用。阿托伐他汀、辅酶Q10均可通过影响Fas/FasL系统、影响细胞凋亡而对心衰起到一定作用。
Objective: To investigate the effect of atorvastatin on Fas / FasL system and the effect of coenzyme Q10 during chronic heart failure. Methods: Adriamycin was intraperitoneally injected into rat heart failure model (2.5 mg / kg, three times a week for 2 weeks) .30 Wistar rats were divided into blank group (6) and heart (N = 24). After 2 weeks of treatment, the rats in HF group were randomly divided into three groups: heart failure group, atorvastatin treatment group [3.75 mg / (kg · d)], coenzyme Q10 Treatment group [2.8 mg / (kg.d)], combined treatment group, continuous gavage for 2 months. The cardiac function of rats was detected by ultrasound, the level of Fas and FasL protein in myocardium was detected by immunohistochemistry and the apoptosis of rat myocardial cells was observed. Results: Compared with the blank group, the rest of the groups had different degrees of cardiac dysfunction, myocardial apoptosis, Fas and FasL protein expression increased, the most obvious heart failure group. Compared with the HF group, the number of apoptotic cells in the three treatment groups decreased, the expression of Fas and FasL protein decreased, and the combined treatment group was further reduced than the single treatment group. Conclusion: The expression of Fas and FasL in heart tissue of rats with heart failure is increased. The Fas / FasL system plays an important role in the process of the heart from compensatory hypertrophy to heart failure. Atorvastatin, coenzyme Q10 can affect the Fas / FasL system, affecting apoptosis and play a role in heart failure.