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Subject Area

Parasitology

Article Type

Original Study

Abstract

Background: Schistosomiasis is a prominent neglected tropical disease that is caused by Schistosoma mansoni, and it is characterized by granuloma formation, which advances to hepatic fibrosis and serious liver damage. The standard medication is praziquantel (PZQ), but it has minimal effect on larvae and no effect on fibrosis which is a main pathological feature in schistosomiaiss. So, new alternatives were suggested, such as sodium butyrate (SB), which is a fatty acid salt with medicinal qualities.

Objective: This study investigated the anti-fibrotic effect of sodium butyrate (SB) in a mouse model of S. mansoni-induced liver immunopathology using parasitological, biochemical, histological, and immunohistochemical (IHC) evaluations.

Methodology: Sixty female BALB/c mice were organized into six groups: GI (normal control), GII (infected, untreated), GIII (normal, SB-treated), GIV (infected, PZQ-treated), GV (infected, SB-treated), and GVI (infected, combined-treated). Worm burden, liver egg count, intestinal oogram, liver enzymes, liver histopathology, and high mobility group box 1 (HMGB1) expression were assessed.

Results: Combination therapy demonstrated the greatest reduction in total worm burden (61%) and hepatic egg count (1876.2 ± 434.50), with significant improvement in liver enzyme levels. Histopathological examination revealed a marked reduction in granuloma number (58.86%) and size (35.9%), accompanied by suppression of HMGB1 expression compared with monotherapies.

Conclusion: Although SB exhibited limited antiparasitic activity, it showed significant anti-fibrotic effects and may serve as a beneficial adjunct to praziquantel therapy.

Creative Commons License

Creative Commons Attribution 4.0 International License
This work is licensed under a Creative Commons Attribution 4.0 International License.

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