OBJECTIVE: To investigate the changes of the two- pore K+ channel TASK-1 in diabetic rats with myocardial injury. METHODS: Thirty-six SD rats were divided into normal group (N), diabetes at 4 weeks (DM 4W) group, and diabetes at 8 weeks (DM 8W) group. The cardiac functions of the rats were determined using cardiac ultrasonography, and the body weight and heart weight of the rats at different time points were measured to calculate the heart/body weight ratio (HW/BW). Myocardial fibrosis in the rats was assessed using Masson's staining. The protein expression of TASK-1 in the myocardium was detected using Western blotting. Whole- cell patch clamp technique was used to record the action potential duration (APD) and twopore domain potassium channel TASK- 1 current in acutely isolated rat ventricular myocytes. meanwhile, The inhibition of TASK-1 current was observed by the TASK-1 specific inhibitor ML-365. RESULTS: Compared with the normal group, the diabetic rats showed significantly increased HW/BW (P < 0.05), end- diastole left ventricular diameter (LVIDd), end- systolic left ventricular diameter (LVIDs), and TASK-1 protein expression, with obviously decreased left ventricular diameter shortening rate (FS) and ejection fraction (EF) (P < 0.01). Masson staining showed that in diabetic rats, the collagen fibers were thickened, interwoven into a network with uneven arrangement and increased deposition. Compared with DM 4W group, the rats in DM 8W group exhibited progressive increases in LVIDd, LVIDs, HW/BW, and TASK-1 expression (P < 0.01 or 0.05); FS and EF were further decreased (P < 0.01). Masson staining showed worsened morphological changes of the myocardium with increased deposition. Compared with that in the normal group, the current of TASK- 1 in diabetic rats at 8 weeks was significantly reduced (P < 0.01) and the duration of action potential was extended (P < 0.05). The TASK-1 current was successfully inhibited by ML-365. CONCLUSIONS: Diabetes can induce myocardial fibrosis and aggravate myocardial injury possibly in relation to changes in the protein expression and current of the two-port potassium channel TASK-1.
OBJECTIVE: To investigate the changes of the two- pore K+ channel TASK-1 in diabeticrats with myocardial injury. METHODS: Thirty-six SD rats were divided into normal group (N), diabetes at 4 weeks (DM 4W) group, and diabetes at 8 weeks (DM 8W) group. The cardiac functions of the rats were determined using cardiac ultrasonography, and the body weight and heart weight of the rats at different time points were measured to calculate the heart/body weight ratio (HW/BW). Myocardial fibrosis in the rats was assessed using Masson's staining. The protein expression of TASK-1 in the myocardium was detected using Western blotting. Whole- cell patch clamp technique was used to record the action potential duration (APD) and twopore domain potassium channel TASK- 1 current in acutely isolated rat ventricular myocytes. meanwhile, The inhibition of TASK-1 current was observed by the TASK-1 specific inhibitor ML-365. RESULTS: Compared with the normal group, the diabeticrats showed significantly increased HW/BW (P &lt; 0.05), end- diastole left ventricular diameter (LVIDd), end- systolic left ventricular diameter (LVIDs), and TASK-1 protein expression, with obviously decreased left ventricular diameter shortening rate (FS) and ejection fraction (EF) (P &lt; 0.01). Masson staining showed that in diabeticrats, the collagen fibers were thickened, interwoven into a network with uneven arrangement and increased deposition. Compared with DM 4W group, the rats in DM 8W group exhibited progressive increases in LVIDd, LVIDs, HW/BW, and TASK-1 expression (P &lt; 0.01 or 0.05); FS and EF were further decreased (P &lt; 0.01). Masson staining showed worsened morphological changes of the myocardium with increased deposition. Compared with that in the normal group, the current of TASK- 1 in diabeticrats at 8 weeks was significantly reduced (P &lt; 0.01) and the duration of action potential was extended (P &lt; 0.05). The TASK-1 current was successfully inhibited by ML-365. CONCLUSIONS:Diabetes can induce myocardial fibrosis and aggravate myocardial injury possibly in relation to changes in the protein expression and current of the two-port potassium channel TASK-1.
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