OBJECTIVES: This study was designed to evidence the protective effect of glucocorticoid therapy on cardiac dysfunction after coronary microembolization (CME), and to clarify its mechanism with the expression of transforming growth factor-beta 1 (TGF-β1)/Smad3 and connective tissue growth factor (CTGF). METHODS: Eighteen mini-pigs were studied, including Sham-operation group (n=4), CME group (n=8) and Glucocorticoid therapy group (n=6, received methylprednisolone 25mg/kg intravenously 30 min before CME). Magnetic resonance imaging (3.0-T) was performed at baseline, 6th hour and one week after operation to evaluate cardiac function. Serum TGF-β1, CTGF and troponin T were also detected. Myocardial expressions of TGF-β1, CTGF and Smad3 were detected by western blot and immunohistochemistry. Total collagen expression was demonstrated by Masson Trichrome stain. RESULTS: Compared with Sham-operation group, left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV) in CME group were increased at 6th hour after CME, while left ventricular ejection fraction (LVEF) was decreased significantly. Compared with CME group, methylprednisolone greatly improved LVEF after CME (6th hour: 56.0 ± 3.2% vs. 51.8 ± 3.8%, P=0.030; one week: 57.8 ± 3.2% vs. 54.6 ± 2.6%, P=0.053). We found that methylprednisolone not only significantly decreased serum TGF-β1, CTGF and troponin T, but also reduced myocardial expressions of TGF-β1, CTGF and Smad3 after CME. In addition, collagen volume fraction in glucocorticoid therapy group was markedly lower than that in CME group. CONCLUSIONS: Glucocorticoid therapy could improve early cardiac function after CME, and its mechanism could be associated with TGF-β1/Smad3 and CTGF suppression.
OBJECTIVES: This study was designed to evidence the protective effect of glucocorticoid therapy on cardiac dysfunction after coronary microembolization (CME), and to clarify its mechanism with the expression of transforming growth factor-beta 1 (TGF-β1)/Smad3 and connective tissue growth factor (CTGF). METHODS: Eighteen mini-pigs were studied, including Sham-operation group (n=4), CME group (n=8) and Glucocorticoid therapy group (n=6, received methylprednisolone 25mg/kg intravenously 30 min before CME). Magnetic resonance imaging (3.0-T) was performed at baseline, 6th hour and one week after operation to evaluate cardiac function. Serum TGF-β1, CTGF and troponin T were also detected. Myocardial expressions of TGF-β1, CTGF and Smad3 were detected by western blot and immunohistochemistry. Total collagen expression was demonstrated by Masson Trichrome stain. RESULTS: Compared with Sham-operation group, left ventricular end-systolic volume (LVESV) and left ventricular end-diastolic volume (LVEDV) in CME group were increased at 6th hour after CME, while left ventricular ejection fraction (LVEF) was decreased significantly. Compared with CME group, methylprednisolone greatly improved LVEF after CME (6th hour: 56.0 ± 3.2% vs. 51.8 ± 3.8%, P=0.030; one week: 57.8 ± 3.2% vs. 54.6 ± 2.6%, P=0.053). We found that methylprednisolone not only significantly decreased serum TGF-β1, CTGF and troponin T, but also reduced myocardial expressions of TGF-β1, CTGF and Smad3 after CME. In addition, collagen volume fraction in glucocorticoid therapy group was markedly lower than that in CME group. CONCLUSIONS: Glucocorticoid therapy could improve early cardiac function after CME, and its mechanism could be associated with TGF-β1/Smad3 and CTGF suppression.