| Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa B |
| Paper ID : 1087-ISCH |
| Authors |
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Ola Ibrahim Rozik *1, Soad Nady2, Manal Mahmoud Hussein2, Ahmed Salem El- Elebiarie2 1Department of Zoology, and Entomology, Faculty of Science, Helwan University, Cairo, Egypt 2Department of Zoology and Entomology, Faculty of Science, Helwan University, Cairo, Egypt |
| Abstract |
| Liver fibrosis is a persistent inflammatory liver disorder that contributes to a variety of conditions, including schistosomiasis. Finding effective therapeutic targets is a crucial need. There are several studies on natural products, such as bee venom and its bioactive substances like melittin (MEL), for the treatment of inflammatory disorders. The therapeutic effect of MEL in a BALB/c mouse model of Schistosoma mansoni-induced liver fibrosis was studied in this research. 48 male BALB/c mice were classified into: a healthy control and five groups infected subcutaneously with cercariae of S. mansoni. The infected groups classified into the infected control, Praziquantel (PZQ)-treated, and MEL-treated groups that received three different doses for 14 days. Hepatic granuloma index (GI) was measured, and serum TNF-α, IL-17, IL-10, and IgE were measured by ELISA. Expressions of STAT3 and NF-κB were assessed. Histopathology of the liver and spleen were also investigated. S. mansoni-infected mice showed significant (P<0.05) increases in the proinflammatory mediators and upregulate expression of STAT3, and NF-κB compared with the healthy group. MEL exhibited anti-inflammatory effects, as evidenced by significant (P<0.05) inhibition of the pro-inflammatory cytokines as well as immunoglobulin E levels and hepatic GI, while the anti-inflammatory IL-10 was significantly (P<0.05) increased. MEL treatment significantly (P<0.05) inhibited the expression of STAT3 and NF-κB insplenocytes compared with healthymice.Themostpositiveeffectswere associated with MEL were observed at the maximum dose. According to the findings, MEL alleviates the degree of hepatic inflammation in a mouse model of S. mansoni-induced liver fibrosis by modulating inflammation through suppression of STAT3 and NF-κB. |
| Keywords |
| anti-inflammatory, liver fibrosis, melittin, nuclear factor kappa B, signal transducer and activator of transcription 3 |
| Status: Abstract Accepted (Oral Presentation) |