Background
Natural venoms have recently demonstrated significant potential in treating diseases         Alzheimer's, hypertension, heart failure, and parasitic infections. Schistosomiasis main issue arises after the deposition of eggs by adult worms, triggering an immunologic granulomatous reaction leads to hepatic failure.
Objective
This study aimed to evaluate the ability of scorpion Leiurus quinquestriatus (SV) and bee, Apis mellifera (BV) venoms to diminish worm load, reduce hepatic inflammatory responses and enhance liver function recovery following S. mansoni injury.
Methods
 Sixty Swiss albino mice were divided into two groups: a negative control group (n=10), and a second group exposed to 65 ± 5 S. mansoni cercariae via subcutaneous injection (n=50) classified into 5 subgroups (10 mice each); one was left as a positive control, while the remaining four received treatments of SV at 0.1 mg/kg/week, SV followed by BV at 0.1 mg each/kg/week, a mixed dose of SV and BV at 0.1 mg each/kg/week, and SV followed by BV at 0.2 mg each/kg/week, respectively, administered once weekly for two weeks. At the end of the ninth week, mice were sacrificed for analysis of blood hematological parameters, liver tissue oxidative stress, worm load, liver histopathology and serum inflammatory cytokines.
Results and conclusion
 The data indicated a significant reduction in nitric oxide (NO) and malondialdehyde (MDA) levels, suggesting a decrease in oxidative stress in liver tissues. Serum levels of Tumor Necrosis Factor Alpha (TNF-α), Interferon-gamma (IFN-γ), Transforming Growth Factor Beta (TGF-β), Interleukin-1 (IL-1), and Interleukin-6 (IL-6) also showed a gradual decrease compared to the infected untreated group due to the treatment. Significant reduction in worm load and oogram pattern was observed followed by Improvements in liver sections and a reduction in granulomatous formation were observed with higher treatment concentrations. Synergistic administration of SV and BV demonstrates remarkable therapeutic potential in mitigating schistosomal infection-induced pathogenesis through comprehensive hepatoprotective mechanisms, including inflammatory modulation, functional hepatic restoration, and tissue regenerative processes.