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目的:观察比索洛尔对心力衰竭大鼠心肌肌浆网钙ATP酶2a(SERCA2a)活性的影响。方法:采用阿霉素腹腔注射法建立大鼠心力衰竭模型,随机分为正常对照组、假手术组、模型组、比索洛尔组、卡托普利组和比索洛尔+卡托普利组,分别以蒸馏水、比索洛尔、卡托普利、比索洛尔+卡托普利连续灌胃35d。观察大鼠心功能指标,ELISA法检测血浆脑钠肽水平,茎环状引物实时定量PCR检测心肌miR-25-3p表达水平,Western blot检测心肌SERCA2a和PLB蛋白表达水平,定磷法测定心肌SERCA2a活性。结果:比索洛尔组、卡托普利组和比索洛尔+卡托普利组大鼠心功能指标明显高于模型组,血浆脑钠肽水平明显低于模型组,miR-25-3p表达水平明显低于模型组,SERCA2a和受磷蛋白(PLB)蛋白表达水平明显高于模型组(P<0.01)。比索洛尔组和比索洛尔+卡托普利组SERCA2a/PLB比值和SERCA2a活性明显高于模型组(P<0.01或P<0.05),卡托普利组与模型组比较无明显差异。结论:比索洛尔可以改善心力衰竭大鼠心功能,机制可能与下调心肌miR-25-3p表达水平,提高SERCA2a、PLB表达水平,提升SERCA2a/PLB比值,增强SERCA2a活性有关。
Objective: To observe the effect of bisoprolol on cardiac sarcoplasmic reticulum calcium ATPase 2a (SERCA2a) activity in heart failure rats. Methods: Adriamycin intraperitoneal injection was used to establish the model of heart failure in rats. The models were randomly divided into normal control group, sham operation group, model group, bisoprolol group, captopril group and bisoprolol + captopril group , Respectively, with distilled water, bisoprolol, captopril, bisoprolol + captopril continuous gavage 35d. The level of plasma brain natriuretic peptide was measured by ELISA. The expression of miR-25-3p in myocardium was detected by real-time quantitative PCR with stem-loop primers. Serum SERCA2a and PLB protein expression were detected by Western blot. The levels of SERCA2a active. Results: The cardiac function of rats in the bisoprolol group, captopril group and bisoprolol + captopril group was significantly higher than that in the untreated group, and the level of plasma brain natriuretic peptide was significantly lower than that in the model group. The expression of miR-25-3p The level of SERCA2a and phosphoprotein (PLB) was significantly lower in model group than in model group (P <0.01). SERCA2a / PLB ratio and SERCA2a activity were significantly higher in the bisoprolol group and the bisoprolol + captopril group than those in the model group (P <0.01 or P <0.05). There was no significant difference between the captopril group and the model group. CONCLUSION: Bisoprolol can improve cardiac function in heart failure rats. The mechanism may be related to down-regulating the expression of miR-25-3p, increasing the expression of SERCA2a and PLB, increasing the SERCA2a / PLB ratio and enhancing the activity of SERCA2a.