Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa B
Background/aim Liver fibrosis is a persistent inflammatory liver disorder that contributes to a wide variety of conditions, including schistosomiasis. There is no approved therapy for liver fibrosis to date; therefore, finding effective therapeutic targets is a crucial need. There are several studie...
Saved in:
| Main Authors: | , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wolters Kluwer Medknow Publications
2024-12-01
|
| Series: | Journal of the Arab Society for Medical Research |
| Subjects: | |
| Online Access: | https://journals.lww.com/10.4103/jasmr.jasmr_23_24 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1841560251010121728 |
|---|---|
| author | Ola I. Rozik Manal M. Hussein Ahmed S. El-elebiarie Soad Nady |
| author_facet | Ola I. Rozik Manal M. Hussein Ahmed S. El-elebiarie Soad Nady |
| author_sort | Ola I. Rozik |
| collection | DOAJ |
| description | Background/aim
Liver fibrosis is a persistent inflammatory liver disorder that contributes to a wide variety of conditions, including schistosomiasis. There is no approved therapy for liver fibrosis to date; therefore, 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.
Materials and methods
Forty-eight male BALB/c mice were classified into six groups (eight mice each): a healthy control group and five groups infected subcutaneously with cercariae of S. mansoni. The infected groups were classified into the infected control group, the Praziquantel (PZQ)-treated group, and three MEL-treated groups that received three different doses (0.1, 0.2, and 0.3 mg/kg, respectively) for 14 days. Hepatic granuloma index (GI) was measured in each experimental mouse, and serum tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), interleukin-10 (IL-10), and immunoglobulin E were measured by ELISA techniques. Additionally, expressions of signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NF-κB) were assessed in splenocytes. Moreover, histopathology of the liver and spleen were also investigated.
Results
S. mansoni-infected mice showed significant (P<0.05) increases in the pro-inflammatory mediators and upregulate expression of STAT3, and NF-κB compared with the healthy group. MEL exhibited potent anti-inflammatory effects, as evidenced by significant (P<0.05) inhibition of the elevated pro-inflammatory cytokines, including TNF-α and IL-17, as well as immunoglobulin E levels and hepatic GI, while the anti-inflammatory IL-10 was significantly (P<0.05) increased. In addition, MEL treatment significantly (P<0.05) inhibited the expression of STAT3 and NF-κB in splenocytes compared with healthy mice. The most positive effects were associated with MEL were observed at the maximum dose.
Conclusion
According to the findings of this study, 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. |
| format | Article |
| id | doaj-art-0bdb69c2e3f4444ba727ec82ed3c48f8 |
| institution | Kabale University |
| issn | 1687-4293 |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Wolters Kluwer Medknow Publications |
| record_format | Article |
| series | Journal of the Arab Society for Medical Research |
| spelling | doaj-art-0bdb69c2e3f4444ba727ec82ed3c48f82025-01-04T14:00:17ZengWolters Kluwer Medknow PublicationsJournal of the Arab Society for Medical Research1687-42932024-12-0119220021010.4103/jasmr.jasmr_23_24Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa BOla I. RozikManal M. HusseinAhmed S. El-elebiarieSoad NadyBackground/aim Liver fibrosis is a persistent inflammatory liver disorder that contributes to a wide variety of conditions, including schistosomiasis. There is no approved therapy for liver fibrosis to date; therefore, 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. Materials and methods Forty-eight male BALB/c mice were classified into six groups (eight mice each): a healthy control group and five groups infected subcutaneously with cercariae of S. mansoni. The infected groups were classified into the infected control group, the Praziquantel (PZQ)-treated group, and three MEL-treated groups that received three different doses (0.1, 0.2, and 0.3 mg/kg, respectively) for 14 days. Hepatic granuloma index (GI) was measured in each experimental mouse, and serum tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), interleukin-10 (IL-10), and immunoglobulin E were measured by ELISA techniques. Additionally, expressions of signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NF-κB) were assessed in splenocytes. Moreover, histopathology of the liver and spleen were also investigated. Results S. mansoni-infected mice showed significant (P<0.05) increases in the pro-inflammatory mediators and upregulate expression of STAT3, and NF-κB compared with the healthy group. MEL exhibited potent anti-inflammatory effects, as evidenced by significant (P<0.05) inhibition of the elevated pro-inflammatory cytokines, including TNF-α and IL-17, as well as immunoglobulin E levels and hepatic GI, while the anti-inflammatory IL-10 was significantly (P<0.05) increased. In addition, MEL treatment significantly (P<0.05) inhibited the expression of STAT3 and NF-κB in splenocytes compared with healthy mice. The most positive effects were associated with MEL were observed at the maximum dose. Conclusion According to the findings of this study, 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.https://journals.lww.com/10.4103/jasmr.jasmr_23_24anti-inflammatoryliver fibrosismelittinnuclear factor kappa bsignal transducer and activator of transcription 3 |
| spellingShingle | Ola I. Rozik Manal M. Hussein Ahmed S. El-elebiarie Soad Nady Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa B Journal of the Arab Society for Medical Research anti-inflammatory liver fibrosis melittin nuclear factor kappa b signal transducer and activator of transcription 3 |
| title | Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa B |
| title_full | Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa B |
| title_fullStr | Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa B |
| title_full_unstemmed | Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa B |
| title_short | Melittin ameliorates schistosomiasis-induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa B |
| title_sort | melittin ameliorates schistosomiasis induced liver fibrosis by suppressing signal transducer and activator of transcription 3 and nuclear factor kappa b |
| topic | anti-inflammatory liver fibrosis melittin nuclear factor kappa b signal transducer and activator of transcription 3 |
| url | https://journals.lww.com/10.4103/jasmr.jasmr_23_24 |
| work_keys_str_mv | AT olairozik melittinamelioratesschistosomiasisinducedliverfibrosisbysuppressingsignaltransducerandactivatoroftranscription3andnuclearfactorkappab AT manalmhussein melittinamelioratesschistosomiasisinducedliverfibrosisbysuppressingsignaltransducerandactivatoroftranscription3andnuclearfactorkappab AT ahmedselelebiarie melittinamelioratesschistosomiasisinducedliverfibrosisbysuppressingsignaltransducerandactivatoroftranscription3andnuclearfactorkappab AT soadnady melittinamelioratesschistosomiasisinducedliverfibrosisbysuppressingsignaltransducerandactivatoroftranscription3andnuclearfactorkappab |