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目的:观察福莫特罗(FORM)对离体培养SD大鼠心肌组织的损伤作用及合用布地奈德(BUD)的影响,初步探讨FORM致心肌损伤的机制。方法:以0μmol/L、0.01μmol/L、0.05μmol/L、0.1μmol/L、0.5μmol/L、1μmol/L、5μmol/L FORM单独及联合10μmol/L的BUD作用于成年SD大鼠离体心脏组织,并培养72 h。ELISA检测组织培养上清液中肌钙蛋白I(cTnI)和心型脂肪酸结合蛋白(H-FABP)含量,RT-PCR检测心脏组织糖原合成酶激酶-3β(GSK-3β),Western blot检测肌浆网钙泵(SERCA2)、GSK-3β蛋白表达水平。结果:(1)组织培养上清液中,cTnI、H-FABP蛋白随着FORM浓度的升高而增加,除外高浓度的两组,各组间差异有统计学意义(P<0.05)。与单独应用相应浓度的FORM比较,联用BUD后cTnI、H-FABP蛋白浓度降低(P<0.05)。(2)随着FORM浓度的升高,SERCA2蛋白表达降低(P<0.05),GSK-3β蛋白表达增高(P<0.05),但GSK-3βmRNA表达无统计学差异。结论:(1)FORM可致心肌损伤,且呈浓度依赖性,联合应用BUD对FORM所致的心肌损伤有保护作用。(2)FORM导致心肌组织损伤的机制与GSK-3β介导的SERCA2蛋白表达量降低有关。
OBJECTIVE: To observe the effect of formoterol (FORM) on myocardial injury in isolated rat SD rats and the effect of budesonide (BUD), and to explore the mechanism of FORM induced myocardial injury. Methods: Adult SD rats were treated with BUD alone or in combination with 10 μmol / L FORM at 0μmol / L, 0.01μmol / L, 0.05μmol / L, 0.1μmol / L, 0.5μmol / L, 1μmol / L and 5μmol / Body heart tissue and cultured for 72 h. The levels of cardiac troponin I (cTnI) and cardiac-type fatty acid binding protein (H-FABP) in the tissue culture supernatants were detected by ELISA. The cardiac glycogen synthase kinase-3β (GSK-3β) Sarcoplasmic reticulum calcium pump (SERCA2), GSK-3β protein expression levels. Results: (1) The cTnI and H-FABP protein in the tissue culture supernatant increased with the increase of the concentration of FORM. Except for the high concentrations, the differences between the two groups were statistically significant (P <0.05). The concentration of cTnI and H-FABP in combination with BUD decreased (P <0.05) compared with that of FORM alone. (2) With the increase of FORM concentration, SERCA2 protein expression decreased (P <0.05) and GSK-3β protein expression increased (P <0.05), but GSK-3βmRNA expression had no statistical significance. Conclusion: (1) FORM can cause myocardial damage, and in a concentration-dependent manner, the combination of BUD has a protective effect on myocardial injury induced by FORM. (2) The mechanism of FORM-induced myocardial injury is related to the decrease of SERCA2 protein expression mediated by GSK-3β.