氟伐他汀对大鼠缺血再灌注损伤心肌eNOS和SERCA活性的影响

目的探讨氟伐他汀对大鼠心肌缺血再灌注损伤的影响和可能机制。方法将老年健康雄性SD大鼠随机分为假手术组、缺血再灌注组、氟伐他汀预处理组,各组再灌注2h后血清检测一氧化氮(NO)含量和内皮型NO合酶(eNOS)活性、血清心肌型肌酸激酶同工酶(CK-MB)和心肌肌钙蛋白(cTnI)水平和心肌肌浆网钙泵(SERCA)活性。结果与缺血再灌注组比较,氟伐他汀预处理组血清NO含量升高(20.14±3.99)μmol/L(P<0.05),eNOS活性明显增加(15.00±3.02)ng/(LP<0.05);血清CK-MB水平降低(1350.11±43.02)IU/(LP<0.05),血清cTnI水平降低(1.73±0.33)μg/(LP<0.05);SERCA活性升高(3.32±0.31)μmol/(mg·prot·h()P<0.05)。结论氟伐他汀能增加NO水平、eNOS和SERCA活性,有效减轻缺血再灌注心肌损伤,其机制可能与保护内皮细胞、减轻细胞内钙超载有关。

Objective To investigate the effect and possible mechanism of fluvastafin,on myocardial ischcmia rcpcrfusion injury. Methods Aged healthy male SD rats were randomly divided into fake operation group, ischemia reperfusion group, fluvastatin pretreatment group. After all the groups were perfused asecond time for two hours, examined the blood serum for nilric oxide （NO） content, the nitric oxide synthase （eNOS） activity, the creatine kinase-MB （CK-MB）, the cardiac troponin I （cTrd） and the sareoplasmic reticulum Ca^2＋-ATPase （SERCA） activity. Results Compared with ischemia reperfusion group, the NO of blood serum in fluvastatin pretrealrnent group was higher（P〈0.05）, and the activity of eNOS was significantly higher（P〈0.05）; the level of CK-MB and cTnI was lower（P〈0.05）; the activity of SERCA was higher（P〈0.05）. Conclusion Fluvastatin can increase the NO level and the activity of eNOS and SERCA, and lessen the ischemia reperfusion injury. Its mechanism maybe is related to protecting endothelial cells and reducing cell calcium overload.