Abstract
This study evaluated the possible antifibrotic effect of pentoxifylline on experimentally induced schistosomal hepatic fibrosis and its effect on serum leptin and transforming growth factor-β1 levels as possible antifibrotic mechanisms in correlation with the hepatic fibrosis indices. A total of ninety clean laboratories bred, males Swiss, albino mice were included, of which ten mice served as a control non-infected, non-treated group and sacrificed at one time. Eighty mice, each was subcutaneously infected with 50 Schistosoma mansoni cercariae and classified into groups: GI (infected & non-treated), GII (infected & treated with Mirazid), GIII (infected & treated with Pentoxifylline) and GIV (infected & treated with a combination of Mirazid and Pentoxifylline). Each group was further subdivided into 2 subgroups; subgroup 'a' which started treatment at 6th week post-infection (P.I.) and sacrificed at the end of 9th week P.I and subgroup 'b' which started treatment at 14th week P.I and sacrificed at the end of 17th week P.I. The efficacy of the treatment was assessed by histopathological examination of the liver with measurement of granuloma sizes, estimation of hydroxyproline content in the liver, and assessment of serum levels of leptin and transforming growth factor- β1 (TGF-β1).Mirazid (MZD) caused significant reductions in granuloma sizes and hepatic hydroxyproline content and caused non-significant reductions in serum levels of leptinand transforming growth factor- β1 t 9th & 17t hweeks P.II(GIII. Pentoxifylline (PTX) caused significant reductions in granuloma sizes, hepatic hydroxyproline, and serum levels of leptin and transforming growth factor- β1 t the 9"th& 17kt weeks P.II (GIII. While combined therapy of both MZD & PTX in GIIVcaused more reductions in granuloma sizes, hepatic hydroxyproline, and serum levels of leptin and TGF- β1 t the 9th & 17th weeks P.IIwhen compared to the other groups.
Published Version
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