Abstract
Obstructive jaundice damages critical functions in the liver. Nitric oxide modulation would influence liver damage induced by biliary obstruction, and little is known about it Acute cholestasis was induced by bile duct ligation (BDL) in two groups of male Sprague-Dawley rats. L-Arginine or serum physiologic was administered to treatment and control group. Histopathological and immunohistochemical iNOS expression was investigated in hepatic tissue. Plasma enzyme activities were increased in acute cholestasis, and that L-arginine treatment partially but significantly prevented the elevation of these markers of liver damage (P < .05). Also histopathology scoring showed that the liver injury was prevented and immunohistochemical iNOS activity was increased significantly in L-arginine group (P < .05). This study shows that, after 7 days of biliary obstruction, liver damage is well established and exogenous L-arginine treatment partially but significantly prevented the liver injury in acute cholestasis.
Highlights
Biliary obstruction is a common surgical problem
The roles of Nitric oxide (NO) in liver damage induced by ischemia reperfusion [4], alcohol [5], dimethylnitrosamine [6], and immunological [7] liver injury have been studied, the function of NO in liver damage induced by bile duct ligation in the rat has not been ascertained
We have studied the effects of exogenous Larginine on the production of NO by regulating the expression of inducible nitric oxide syntheses (iNOS) proteins
Summary
Despite the advances in diagnostic and therapeutic modalities, its morbidity and mortality are high. Cardiovascular dysfunction, peripheral vasoconstriction, renal insufficiency, gastrointestinal hemorrhage, coagulopathy, and sepsis are major complications that affect its morbidity and mortality [1]. According to experimental and clinical studies, these complications develop because of hypotension, immunosuppression, hepatic dysfunction, and high serum levels of toxic substances such as bile salts and endotoxin [1]. The synthesis of NO from L-arginine is known to exist in a number of cells, including endothelial cells, macrophages, cerebellar neurons, neutrophils, Kupffer cells, and hepatocytes [2]. Macrophages and hepatocytes produce much greater quantities of NO, which is not detectable until several hours after exposure to a specific inflammatory or septic stimulus [3]. The roles of NO in liver damage induced by ischemia reperfusion [4], alcohol [5], dimethylnitrosamine [6], and immunological [7] liver injury have been studied, the function of NO in liver damage induced by bile duct ligation in the rat has not been ascertained
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