[Effect of lipid factor CTRP9 on myocardial remodeling induced by isoproterenol in mice]

Objective: To investigate the effect of lipid factor CTRP9 on myocardial remodeling induced by isoproterenol in mice. Methods: Male C57BL/6J mice were randomly assigned to four groups (n=10 per group), then mice were administered 5 mg/kg ISO q12h for 12 days by daily subcutaneous injection to induce myocardial remodeling model. Mice also received subcutaneous injection of CTRP9 (200 μg·kg(-1)·d(-1)) for 12days. Echocardiography was performed to compare the ventricular wall thickness and cardiac function. Heart weight/body weight (HW/BW), lung weight/body weight (LW/BW), heart weight/tibia length (HW/TL) and cross-sectional area of cardiomyocytes were compared between groups. The cardiac hypertrophic markers and fibrotic markers were also compared by RT-PCR between the two groups. Molecular protein changes were evaluated by Western blot. Results: CTRP9 was down-regulated in model group. The LVEDd (4.00 mm vs 4.67 mm), LVEDs (2.60 mm vs 3.12 mm) in mode group were both higher than control group while the LVEF (73% vs 55%) and FS (39% vs 21%) were reduced in mode group. Compared with the control group, the HW/BW, LW/BW, HW/TL and cross-sectional area of cardiomyocytes were much higher in mode group (P<0.05). The transcription level of hypertrophic markers (ANP, BNP, β-MHC) were elevated. Left ventricular collagen volume was increased as well as the transcription level of fibrosis markers collagen Ⅰ, collagen Ⅲ and a-SMA. Western blot results indicated that CTRP9 increased nNOS and eNOS derived NO production but not iNOS expression. Conclusion: CTRP9 could protect against ISO induced myocardial remodeling by increasing nNOS and eNOS derived NO production.