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目的:探讨福辛普利拉对培养乳鼠心肌细胞缺氧/复氧(A/R)损伤的预防作用。方法:取SD新生大鼠(1~3 d),培养成心肌细胞,在培养的第4天随机分为5组:①正常对照组,②A/R组,③0.2 mmol/L福辛普利拉预处理组(F1组),④0.6 mmol/L福辛普利拉预处理组(F2组),⑤1.8 mmol/L福辛普利拉预处理组(F3组)。分别观察各组心肌细胞搏动频率、细胞存活率、培养液中乳酸脱氢酶(LDH)活性、心肌细胞肌浆网钙泵(SERCA)mRNA的表达水平和心肌细胞内游离[Ca2+]浓度。结果:①细胞搏动频率:A/R组比正常对照组明显减低(P<0.01);福辛普利拉各剂量组比A/R组显著加快(P<0.01),比正常对照组稍慢(P>0.05)。②细胞存活率:A/R组比正常对照组明显降低(P<0.01);福辛普利拉各剂量组比A/R组明显增高(P<0.01),而与正常对照组相比差异无统计学意义(P>0.05)。③LDH活性:A/R组比正常对照组明显升高(P<0.01);福辛普利拉各剂量组比A/R组明显降低(P<0.01),与正常对照组相比虽有升高但差异无统计学意义(P>0.05)。④SER-CA mRNA的表达水平:A/R组比正常对照组mRNA表达下调,为正常对照组的(0.78±0.30)倍(P<0.01);福辛普利拉各剂量组比A/R组显著上调(P<0.01)。⑤心肌细胞内游离[Ca2+]浓度:A/R组比正常对照组明显升高(P<0.01);福辛普利拉各剂量组比A/R组明显降低(P<0.01),而与正常对照组相比差异无统计学意义(P>0.05)。结论:福辛普利拉预处理后对A/R心肌细胞损伤具有预防作用,其机制可能与SERCA表达上调、减轻细胞内Ca2+超载有关。
Objective: To investigate the preventive effect of fosinopril on neonatal rat cardiomyocyte hypoxia / reoxygenation (A / R) injury. Methods: SD neonatal rats (1-3 days) were cultured and cultured into cardiomyocytes. They were randomly divided into 5 groups on the 4th day of culture: ① normal control group, ② A / R group, ③ 0.2 mmol / L fosinopril (Group F1), 0.6 mmol / L fosinoprilat pretreatment group (group F2), and ⑤ 1.8 mmol / L fosinopril pretreatment group (group F3). The beating frequency, cell survival rate, lactate dehydrogenase (LDH) activity, expression of cardiomyocyte calcium pump (SERCA) mRNA and intracellular free [Ca2 +] in myocardial cells were observed in each group. Results: ① The frequency of cell pulsation was significantly lower in A / R group than that in normal control group (P <0.01); the dosage of fosinoprilat group was significantly faster than that in A / R group (P <0.01) (P> 0.05). ② The cell viability was significantly lower in the A / R group than in the normal control group (P <0.01), and that in the fosinopril group was significantly higher than that in the A / R group (P <0.01) No statistical significance (P> 0.05). (3) LDH activity: A / R group was significantly higher than the normal control group (P <0.01); Fosinoprilat dose group than A / R group was significantly lower (P <0.01), compared with the normal control group But the difference was not statistically significant (P> 0.05). The expression of SER-CA mRNA in the A / R group was significantly lower than that in the normal control group (0.78 ± 0.30) (P <0.01) Significantly increased (P <0.01). The concentration of free Ca2 + in cardiomyocytes was significantly higher in A / R group than that in normal control group (P <0.01), and in each dose of fosinoprilat group was significantly lower than that in A / R group (P <0.01) The difference between the normal control group was not statistically significant (P> 0.05). CONCLUSION: Fosinopril preconditioning can prevent cardiomyocyte injury in A / R cells. The mechanism may be related to up-regulation of SERCA expression and reduction of intracellular Ca2 + overload.