基于TLR4介导的炎症通路探讨利拉鲁肽对糖尿病大鼠心肌的保护机制

目的 基于Toll样受体4(TLR4)介导的炎症通路研究利拉鲁肽对糖尿病大鼠心肌的保护机制.方法 36只SD大鼠随机分为对照组、糖尿病组、干预组,每组12只,糖尿病组和干预组腹腔注射60 mg/kg链脲佐菌素(STZ)溶液以制备糖尿病大鼠模型,造模成功后干预组给予200 μg·kg1·d-1利拉鲁肽腹腔注射,糖尿病组和...

Study on the protective mechanism of lilarupeptide on myocardium of diabetic rats based on TLR4-mediated in-flammatory pathway

Objective To investigate the effect of liraglutide on inflammatory pathway in diabetic rats and its protec-tive mechanism against myocardial injury.Methods36 SD rats were randomly divided into three groups and received thecorresponding treatments,namely,control group,diabetic group and intervention group,each with 12 cases. After 8 weeksof continuous intervention,the general condition of each group was observed. The biochemical parameters were detected,in-cluding low density lipoprotein(LDL),high density lipoprotein(HDL),triglyceride(TG),total cholesterol(TC)and glu-cose(Glu). The myocardial systolic function related indexes were also detected,including left ventricular ejection fraction(LVEF),left ventricular fractional shortening(LVFS),stroke output(SV). The pathological changes of myocardium wereobserved,and the expression levels of Toll-like receptor 4(TLR4),myeloid differentiation factor 88(My D88)and nuclearfactor κB(NF-κB)p65 in myocardium were detected.ResultsHE staining showed that the pathological changes of myo-cardium in intervention group were significantly improved compared with diabetic group. TC,TG,LDL and Glu were highestin diabetic group,followed by intervention group and control group(P<0.05). HDL,LVEF,LVFS and SV were lowest indiabetic group,followed by intervention group and control group(P<0.05). The expression levels of TLR4,My D88 and NF-κB p65 protein in myocardial tissue were highest in diabetic group,followed by intervention group and control group(P<0.05).Conclusion Liraglutide may protect the myocardium of diabetic rats by down-regulating the TLR4-mediated inflam-matory pathway in myocardial tissue,thereby improving the myocardial pathological damage and cardiac function,whichmay be a new therapeutic target for diabetic myocardial damage.