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EN
Insulin resistance (IR) plays a critical role in metabolic syndrome (MS). Previous studies have demonstrated that activated ROCK is increased in MS patients. However, the effect of Rho-kinase (ROCK) on IR has not been definitely determined. Thus, the aims of the present study were to determine whether ROCK activation induces IR or affects myocardial structure and function, as well as the possible mechanisms underlying this process. Wistar rats fed high fat, high glucose and high salt diet sewed as model of MS and we used transmission electron microscopy, echocardiogram technology, and terminal deoxynucleotidyl transferase-mediated DNA nick-end labeling staining to identify any myocardial damage. The protein levels of MYPT-1 (characteristic of ROCK activation), IRS-1 and AKT were analyzed by immunohistochemistry and Western blotting. In hearts from MS rats, we found increased protein levels of phospho-MYPT-1 and phospho-IRS-1 (Ser307) and decreased phospho-AKT compared to levels in normal rats. In conclusion, the results suggest that ROCK-mediated IR is involved in the development of myocardial impairments in MS rats and that this effect is mediated probably via the IRS-1/PI3-kinase/AKT pathway.
EN
Inflammation plays an important role in the development of many obesity-related diseases. This study aimed to investigate the effect of ezetimibe on inflammation and myocardial remodeling in obese rats. A rat model of obesity was established, and myocardial damage was examined by transmission electron microscopy and Masson staining. Twenty obese rats were divided into two groups (n=10): obese group and ezetimibe group. Ten SD rats were used as controls. Western blot was performed to monitor the expression of P-p38MAPK and interleukin (IL)-6. Immunohistochemical staining was used to monitor the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. In the obese rats group, we observed increased inflammatory factors and myocardial hypertrophy. In contrast, the ezetimibe group exhibited decreased expression of inflammatory factors and an improvement in myocardial remodeling compared to the obese group. Mechanistically, we found that ezetimibe decreased P-p38MAPK, IL-6, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 levels in the hearts of the obese rats. Taken together, these results indicate that ezetimibe may improve myocardial remodeling in obese rats by inhibiting inflammation.
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