Sophorolipids produced byYarrowia lipolyticagrown onMoringa oleiferaoil cake protect against acetic acid-induced colitis in rats: impact on TLR-4/p-JNK/NFκB-p65 pathway

Author:

Nooman Mohamed U1,Al-kashef Amr S1,Rashad Mona M1,Khattab Abd El-Nasser A2,Ahmed Kawkab A3,Abbas Samah S4ORCID

Affiliation:

1. Biochemistry Department, Biotechnology Research Institute, National Research Centre , Cairo , Egypt

2. Genetics and Cytology Department, Biotechnology Research Institute, National Research Centre , Cairo , Egypt

3. Pathology Department, Faculty of Veterinary Medicine, Cairo University , Cairo , Egypt

4. Pharmacology and Toxicology Department, Faculty of Pharmacy, Misr International University , Cairo , Egypt

Abstract

AbstractObjectivesToll-like receptor-4 (TLR-4) activation plays a major role in triggering oxidative stress (OS) and inflammation implicated in the pathogenesis of ulcerative colitis (UC). Due to sophorolipids (SLs) antioxidant and anti-inflammatory properties, they are interestingly becoming more valued for their potential effectiveness in treating a variety of diseases. This study was designed to explore the effect of SLs produced by microbial conversion of Moringa oleifera oil cake using isolated yeast Yarrowia lipolytica against UC induced by acetic acid (AA) in rats.MethodsThe produced SLs were identified by FTIR, 1H NMR and LC-MS/MS spectra, and administered orally for 7 days (200 mg/kg/day) before AA (2 ml, 4% v/v) to induce UC intrarectally on day eight. Biochemically, the levels of TLR-4, c-Jun N-terminal kinase (JNK), nuclear factor kappa B-p65 (NFκB-p65), interleukin-1beta (IL-1β), malondialdehyd, glutathione, Bax/Bcl2 ratio and the immunohistochemical evaluation of inducible nitric oxide synthase and caspase-3 were assayed.Key findingsSLs significantly reduced OS, inflammatory and apoptotic markers in AA-treated rats, almost like the reference sulfasalazine.ConclusionsThis study provided a novel impact for SLs produced by microbial conversion of M. oleifera oil cake against AA-induced UC in rats through hampering the TLR-4/p-JNK/NFκB-p65 signalling pathway.

Funder

National Research Centre

Publisher

Oxford University Press (OUP)

Subject

Pharmaceutical Science,Pharmacology

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