The Role Of Adiponectin(APN)in Hypertension-induced Cardiac Inflammation And Fibrosis

Objective:To study the role of adiponectin(APN)in hypertension-induced cardiac inflammation and fibrosis.Methods:Wildtype and APN knockout mice(Each of the 12 rats) were divided randomly into4 groups(wildtype control group(6 mice, WT), APN knockout control group(6 mice,APN﹣/-),wildtype angiotensin II infusion group(6 mice, WT+Ang II), APN knockout angiotensin II infusion group( 6 mice, APN﹣/-+Ang II) with angiotensin II(1500ng/min*kg, 7d) or solvent infusion(sham group) respectively. Mouse blood pressure was measured and echocardiography was performed at the 7th day of angiotensin II infusion.Results:At the 7th day of angiotensin II infusion, the blood pressure of angiotensin II infusion group was higher than Sham group, and there was no difference in the wildtype and knockout group after angiotensin II infusion. Using the ELISA method for the determination of serum s ICAM 1, s VCAM 1, v WF endothelial injury of the content of evaluation.The Masson Trichrome staining showed that APN deficiency increased the angiotensin II infusion-induced cardiac fibrosis(p<0.05).Immunohistochemistry staining for α-SMA also showed that knockout of APN increased the α-SMA+ myofibroblast formation. HE staining showed an increase in knockout mice in response to angiotensin II infusion. Compared with the angiotensin II infused wildtype group, the inflammatory cytokines, including TGF-β and TNF-α, secretion was also increased by knockout of APN in response to angiotensin II infusion.ConclusionIn the process of high blood pressure caused by cardiac fibrosis,APN knockout,increase vascular endothelial damage,increase the inflammation factor(TGF-β、TNF-α)secre secretion, leading to heart tissue in alpha SMA + muscle fibroblasts forming,eventually aggravate cardiac fibrosis.