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.