动物造模,2型糖尿病 z-bio 2021-01-29 341

　　OBJECTIVE: To investigate the protective effect of angiotensin Ⅱ receptor blocker irbesartan on myocardial inflammation in type 2 diabetic db/db mice and its cardioprotective mechanism.

　　Method: 10 weeks old db/db mice were randomly divided into model group and irbesartan treatment group at 50mg/(kg·D). 10-week-old non-diabetic db/+ mice born in the same litter served as a normal control group. The normal and model groups were given the same dose of normal saline, while the irbesartan treatment group was given irbesartan (dissolved in saline). After 16 weeks of drug intervention, the heart mass and weight were recorded, and the fasting blood glucose level was recorded. Blood glucose was detected by HE staining, Western blot, immunohistochemistry and cardiac qPCR, and the second trimester and total blood cholesterol content were determined.

　　Results: Compared with the db/+ mice in the normal group, the db/db mice in the model group showed obesity, hyperglycemia and hyperlipidemia (P\u003c0.01); the muscle fibers of the myocardial tissue were arranged randomly with gaps Increased space; and inflamed cell infiltration; increased P-IкBα protein level, decreased IкBα protein level, increased P-IкBα/IкBα (P\u003c0.001); increased NF-κB (P65) activity, increased nuclear invasion (P \u003c0. 001), the pro-inflammatory cytokine interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) mRNA levels are increased (P\u003c0.01), all these abnormalities are related to the increase of inflammatory response related. Diabetic myocardium. The chronic treatment of irbesartan improved myocardial pathological changes caused by hyperglycemia in type 2 diabetic db/db mice, and improved the inflammation index of myocardial tissue.

　　Conclusion: Irbesartan improves myocarditis in type 2 diabetic db/db mice. This mechanism may be related to the inhibition of cardiac angiotensin II and NF-κB signaling pathways.