The Mechanism Research Of Heme Oxygenase 1 In Portal Hypertension

Objective: To verify expression of heme oxygenase 1 protein in liver cirrhosis and portal hypertensive rat model is related with oxida stress.To determine whether nuclear translation of Nrf2 will cause such over-expression.To verify increased HO-1 protein expression results in portal hypertension through causing anomaly blood flows in visceral organs and potential mechanisms.Method: Portal hypertensive rats was induced by CCL4 subcutaneous injection.Western blotting was used to determine Nrf2 and HO-1 expression.DYE-TRAK colored microspheres was used to determine blood flows in visceral organs.Perfusion system was used to determine contractile response of mesenteric arterioles to norepinephrine.Results: Compared with normal rats,HO-1,nuclear Nrf2 expression and portal pressure increased significantly in PHT rats.After anti-oxidative treatment,HO-1 and nuclear Nrf2 expression in mesenteric arteries decreased significantly.Anomaly blood flows and portal pressure in PHT rats would be attenuated by HO-1 inhibitor.PHT rats had low contractile response of mesenteric arterioles to norepinephrine,and after Snpp treatment such response was partly recoverd.Conclusion: Oxidative stress in CCL4 induced portal hypertensive rat model results in over-expression of heme oxygenase 1protein.HO-1 plays an important role in regulation of blood flows in visceral organs and eventually results in portal hypertension.Snpp treatment was capable of reversing abnormal blood flows in visceral organs through recovering contractile response of mesenteric arterioles to norepinephrine.