A bioactive product lipoxin A4 attenuates liver fibrosis in an experimental model by regulating immune response and modulating the expression of regeneration genes

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dc.contributor.authorKurtoğlu, Elçin Latife
dc.contributor.authorKayhan, Başak
dc.contributor.authorGül, Mehmet
dc.contributor.authorKayhan, Burçak
dc.contributor.authorAkdoğan Kayhan, Meral
dc.contributor.authorKaraca, Zeynal Mete
dc.contributor.authorYeşilada, Elif
dc.date.accessioned2021-05-20T08:10:29Z
dc.date.available2021-05-20T08:10:29Z
dc.date.issued2019
dc.departmentİnönü Üniversitesien_US
dc.description.abstractAbstract: Background/Aims: Lipoxin A4 (LXA4), an anti-inflammatory lipid mediator, regulates leukocyte cellular activity and activates gene transcription. The therapeutic effect of LXA4 on liver fibrosis and its mechanism on the immune system are largely unknown. Because the regenerative capacity of hepatocytes in acute and chronic liver failure models of mouse increases by silencing MKK4, we aimed to investigate the effect of parenteral administration of LXA4 on the genes responsible for regeneration of liver, namely MKK4, MKK7, and ATF2, and visualize the therapeutic effects in an experimental model. Materials and Methods: Fibrosis was induced in mice by administration of thioacetamide (TAA). LXA4 was administered during the last two weeks of fibrosis induction. The fibrosis level was measured by Knodell scoring. The liver function was measured by analyzing serum ALT, AST, and AP levels. Expression levels of genes responsible for liver fibrosis (TGF-?) and cell regeneration (MKK4, MKK7, and ATF2) have been measured by RT-PCR analysis. Inflammatory and anti-inflammatory cytokine levels were measured in serum samples and liver homogenates by Enzyme Linked Immunosorbent Assay (ELISA). Ultrathin sections were examined using a transmission electron microscope and analyzed. Results: We observed significant healing in liver of the LXA4-treated group, histologically. This finding was in parallel with reduction of serum ALT, AST, but not AP levels. TGF-? and MKK4 expressions were significantly reduced in the LXA4-treated group. Administration of LXA4 caused significant elevation of IL-10 in systemic circulation; however, that elevation was not detected in liver homogenates. Nevertheless, significant reductions in TNF-? and IL-17 have been observed. Conclusion: The anti-inflammatory effect of LXA4 maintains the regenerative capacity of liver during fibrosis in an experimental liver fibrosis model. LXA4 may be therapeutically beneficial in liver fibrosis.en_US
dc.identifier.citationKURTOĞLU E. L,KAYHAN B,GÜL M,KAYHAN B,KAYHAN M. A,KARACA Z. M,YEŞİLADA E,YILMAZ S (2019). A bioactive product lipoxin A4 attenuates liver fibrosis in an experimental model by regulating immune response and modulating the expression of regeneration genes. Turkish Journal of Gastroenterology, 30(8), 745 - 757. Doi: 10.5152/tjg.2019.18276en_US
dc.identifier.doi10.5152/tjg.2019.18276en_US
dc.identifier.endpage757en_US
dc.identifier.issn1300-4948
dc.identifier.issn2148-5607
dc.identifier.issue8en_US
dc.identifier.pmid31418419en_US
dc.identifier.scopus2-s2.0-85071537250en_US
dc.identifier.scopusqualityQ3en_US
dc.identifier.startpage745en_US
dc.identifier.trdizinid351250en_US
dc.identifier.urihttps://doi.org/10.5152/tjg.2019.18276
dc.identifier.urihttps://hdl.handle.net/11616/33646
dc.identifier.urihttps://search.trdizin.gov.tr/yayin/detay/351250
dc.identifier.volume30en_US
dc.identifier.wosWOS:000481718800011en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakTR-Dizinen_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isotren_US
dc.relation.ispartofTurkish Journal of Gastroenterologyen_US
dc.relation.publicationcategoryMakale - Ulusal Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.titleA bioactive product lipoxin A4 attenuates liver fibrosis in an experimental model by regulating immune response and modulating the expression of regeneration genesen_US
dc.typeArticleen_US

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