| Background: DCM is one of the complications of DM,whose pathology arecardiac hypertrophy and myocardial fibrosis.It is not only can seriously affect the lifequality of patients with diabetes, but also it’s the cause of death in patients. To delaythe development of DCM has far-reaching implications for the treatment of DM.Rutin is one kind of widely distributed flavonoids with strong pharmacologicalactivity and low toxicity. It has protective effects on multiple organs. And it can beused to prevent stroke, hypertension and other cardiovascular diseases in clinic.Objective: Investigate the protective effect and mechanism of rutin onmyocardial fibrosis in type2diabetic rats.Methods:40adult Wistar rats were fed adaptively for1week. Eight of themwere randomly selected as the normal group and given a normal diet, while the restwere given a high fat and sugar diet. The high fat feeding rats were given a singleintraperitoneal injection of a small dose of STZ (25mg/kg) to make the type2diabeticrat model in the tenth week. Then the model rats were randomly divided into modelgroup(1mL/kg0.5%CMC-Na),rutin group(40mg/kg/d),control group (5mg/kg/d), inthe fourteenth week.And they were intervened by intragastric administration(once/day) for4weeks and the fasting blood glucose was measured weekly.Thechange of myocardial structure was observed by HE staining,expression ofmyocardial collagen was evaluated by Masson trichrome staining,expressions of FN,tTG and RockⅠwere analyzed by immunohistochemistry and Western blot.Results:①When observing in general state, rats in normal group had smooth furand shapely body.While in model group,the fur of rats was less luster,with polyphagia,polydipsia and polyuria,as well as significant weight loss. In control group and rutintreatment group,the fur of rats was white and gloss and above three symptoms were relieved.②Determinations of blood glucose showed that blood glucose of normal groupwas stable and maintained at4.9~6.1mmol/L,while the model group was significantlyincreased(P<0.05).Blood glucose of control group and rutin group weredecreased(P<0.05).③Results of HE staining showed that rats in normal group had orderedmyocardial tissue,obvious and regular nuclei,uniform staining without cellularswelling and muscle fibers dissolving.While the rats in model group had disorderedmyocardial tissue,irregular cell,obvious interstitial fibrosis and large intercellularspace.Compared with model group,rats in control group and rutin group had a slightlydisordered myocardial tissue,general complete cell morphology and mild fibrosis.④Results of Masson staining showed that in normal group,the myocardial cellnucleus of rats appeared dark blue,with a few evenly distributed myocardialinterstitial collagen fibers appeared green and the myocardial cytoplasm appeared red.The expression of collagen in myocardial interstitial and around vessel was increasedsignificantly in the model group and also had significant differences compared withthat in normal group(P<0.05),while the myocardial collagen in control group andrutin group were significantly decreased compared with the model group (P<0.05).⑤Results of immunohistochemistry revealed that there were little expressions ofFN,tTG and RockⅠ in myocardial tissue for rats in normal group, while expressionsof FN,tTG and RockⅠin model group were significantly higher than those in innormal group(P<0.05).There were more less expressions in control group and Rutingroup (P<0.05).⑥Western blot results showed that there are little expression of tTG and RockIin normal group,while the expression in model group is increased (P<0.05).Expressions of tTG and RockⅠ in control group and rutin treatment group wasdecreased compared with the model group(P<0.05).Conclusion：1.Rutin can improve the general condition of diabetic rats,decreaseblood glucose by a certain extent,inhibit deposition of myocardial collagen, reduce theinjury of myocardial cells to protect hearts of diabetic rats.2.Rutin can inhibit the overexpression of tTG and FN in myocardial tissue of diabetic rats,downregulate the expression of RockⅠ in Rho/Rock signalpathway,reduce myocardial fibrosis in diabetic rats. |
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