PRANLUKAST EFFECT ON THE EARLY STAGES OF LIVER DAMAGE IN RATS TREATED WITH CCl4

Abstract

Development of liver fibrosis is accompanied by an increased amount of nitric oxide (NO), prostaglandin E2 (PGE2) and 5-lipoxygenase products as leukotrien B4 (LTB4). Carbon tetrachloride (CCL4) induced liver fibrosis in experimental models are often used for investigation of the hepatoprotective effect of drugs. The potential effect of either silymarin and/or pranlukast against CCL4 induced liver damage was examined in a CCL4 model in rats. Sprague Dawley male rats were intraperitoneally injected with CCL4 and received Silymarin and or pranlukast orally once daily for 8 weeks. Both silymarin and pranlukast significantly decreased serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), increased the activities of superoxide dismutase (SOD) and catalase, decreased malondialdehyde (MDA) content in liver and in addition, they decreased (NO) production and transforming growth factor ẞ in CCL4 treated rats compared with CCL4 group.
In conclusion, this study proved that pranlukast protects CCL4 treated rats from liver fibrosis via its ability to decrease oxidative free radicals and transforming growth factor ẞ induced liver fibrosis.