Hepatitis B Virus (HBV)

TNF-a but not IL-1a

TNF-a but not IL-1a

TNF-a but not IL-1a is correlated with PGE1-dependent protection against acute D-galactosamine-induced liver injury

Experimental studies have shown that prostaglandins have protective properties against different models of liver injury. Prostaglandin E (PGE) reduces liver toxicity in­duced by D-galactosamine (D-GalN), thioacetamide, aflatoxin B1, carbon tetrachloride, bile duct ligature, fat-enriched and choline-deficient diet, viral hepati­tis and complement-mediated hepatic necrosis. Fur­thermore, PGE has a beneficial effect on fulminant viral hepatitis in humans, reducing serum transaminase levels and improving encephalopathy and coagulation factors. Prostacyclin also reduces transaminase levels during D-GalN-induced hepatic necrosis.

Different hypotheses have been suggested to explain the protective effect of prostaglandins in liver injury according to the different experimental models used. Among those cited are increased vascularization, reduced plasma membrane microviscosity, modification of the arachidonic acid cascade profile, antifibrotic activity and immunomodulatory activity.

Cytokines and nitric oxide have also been shown to pre­vent liver damage induced by noxious agents. In this sense, D-GalN-treated animals can be protected to an otherwise le­thal challenge of either lipopolysaccharide (LPS) or tumour necrosis factor-alpha (TNF-a) toxicity by pretreatment with TNF-a or interleukin (IL)-1a. Nitric oxide has been implicated in the development of tolerance to LPS- or cytokine-induced toxicity. The present article focuses on the potential involvement of TNF-a, IL-1 a and nitric oxide in the protection obtained with PGE1 against D-GalN-induced injury in liver.
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Category: Main

Tags: Cytokines, D-galactosamine, Hepatotoxicity, Inter- leukin-lalpha, Liver injury, Nitric oxide, Prostaglandin Ei, Tumour necrosis factor-alpha

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