Research Article

Salvianolic Acid B Reducing Portal Hypertension Depends on Macrophages in Isolated Portal Perfused Rat Livers with Chronic Hepatitis

Figure 7

Salvianolic acid B indirectly reduced portal hypertension via NO/CO potency. In portal triads, the smooth muscle cells in terminal portal venules and the sphincter-like endothelia at hepatic sinusoid inlets were relaxed by both of the nitric oxide (NO) from inducible NO synthase (iNOS) or endothelial NO synthase (eNOS) and the carbon monoxide (CO) from heme oxygenase-1 (HO-1). The resistance of intrahepatic portal vein was mainly originated from both cells, since the expanding portal vein in portal triads indicated its backward location, and the narrowed hepatic sinusoids between hepatic cords did its forward location. It was the infiltrated macrophages that make salvianolic acid B (Sal B) effect switching, from its constricting in physiological status into its relaxing terminal portal venules in chronic hepatitis. The mechanisms of Sal B might be exploited from its elevating NO bioavailability and CO potency. (1) Sal B limited NADPH oxidase (NOX2) expression, decreased the superoxide ( ), blocked peroxynitrite (ONOOāˆ’) generation from NO, and inhibited eNOS nitration and inactivation. (2) Sal B promoted iNOS/HO-1 expression and increased NO/CO potency to relax the smooth muscle cells and the sphincter-like endothelia. (3) Sal B might regulate upward the extracellular superoxide dismutase (ecSOD), promoted H2O2 formation from , blocked ONOOāˆ’ generation from NO, then H2O2 enhanced iNOS, HO-1 and ecSOD expression itself. It consisted of a benign cycle (blue lines) against the vicious cycle (red lines).
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