Role of Phosphodiesterase Enzyme Modulation in Protection of Hepatotoxicity Induced by D-Galactosamine in Rats | ||||
Bulletin of Egyptian Society for Physiological Sciences | ||||
Article 18, Volume 29, Issue 1, June 2009, Page 229-244 PDF (631.7 K) | ||||
Document Type: Original Article | ||||
DOI: 10.21608/besps.2009.36343 | ||||
View on SCiNiTO | ||||
Authors | ||||
Magdy Hassan* 1; Mohamed El-Moselhy2; Ashraf Abu-Elwafa2; Hanaa Ibrahim1; Aliaa Mohammed2 | ||||
1Department of Physiology; Faculty of Pharmacy, Minia University | ||||
2Department of Pharmacology & Toxicology Faculty of Pharmacy, Minia University | ||||
Abstract | ||||
The study was conducted to investigate possible mechanisms of the hepatoprotective actions of Pentoxifylline (a non-selective phosphodiesterase inhibitor) against experimentally induced hepatic injury in rats. The rats were randomly assigned to vehicle (saline), pentoxifylline (PTX, 100 mg/Kg) and silymarin (SYM, 100mg/Kg) and combination of the two in the same doses pretreated groups for three weeks, in addition to the control group. Hepatic injury was induced by intraperitoneal single dose injection of D-galactosamine (D-GAL, 800mg\kg). Hepatic functions parameters (serum levels of albumin, and alkaline phosphatase (ALP) activity were determined. Antioxidants properties of pentoxyphylline were examined via measuring the antioxidant enzymes activities such as superoxide dismutase (SOD), catalase (CAT), lipid peroxides as well as hepatic total nitrites. Histopathological findings were, also, determined using portions of liver tissues. Results showed that the liver injury induced by D-galactosamine treated rats was improved in the three pretreated groups to variable extents. Pretreatment with PTX prevented D-galactosamine induced reduction of antioxidative enzymes, SOD and CAT, and attenuated the elevated MDA level in hepatic tissue which was observed in non pretreated D-Gal group. These findings could be attributed to antioxidant activity of PTX and its metabolites effects. It 'also' caused increase in hepatic triglycerides, normalization of nitric oxide level, and lowering serum ALP activity and inhibited reduction of serum albumin level caused by D-Gal, these effects reflect possible hepatoprotective effects of PTX. | ||||
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