Methyl Jasmonate Reduces The Inflammation And Apoptosis Of Hk-2 Cells Induced By Lps By Regulating The Nf-Kappa B Pathway

Background: Methyl jasmonate is a bioactive oxylipid that participates in the defense-related mechanisms of plants. The anti-inflammatory and anti-oxidative capacities of methyl jasmonate against lipopolysaccharide (LPS) induced arthritis have been widely investigated. However, the role of methyl jasmonate in LPS-induced cell model of tubular-interstitial nephritis (TIN) has not been reported.Methods: LPS (5 mu g/mL) was applied to treat human renal tubular epithelial cell line (HK-2) for the establishment of TIN cell model. LPS-induced HK-2 was incubated with 10 or 20 mu M methyl jasmonate, cell viability and apoptosis were assessed by MTT and flow cytometry. ELISA and qRT-PCR were performed to determine the levels of interleukin (IL)-1 beta (IL-1 beta), IL-6, IL-8 and tumor necrosis factor-alpha (TNF-alpha). The downstream pathway was investigated by western blot.Results: LPS induced cytotoxicity in HK-2 cell accompanied by decrease of cell viability and increase of cell apoptosis. Methyl jasmonate dosage dependently enhanced the cell viability and reduced cell apoptosis to ameliorate the cytotoxicity. LPS also induced inflarrunatoty response in HK-2 cell with increased IL-1 beta, IL-6, IL-8 and INF-alpha. Methyl jasmonate attenuated LPS-induced inflammation in HK-2 cell. Protein expression of I kappa B alpha was down-regulated, p65 and I kappa B alpha phosphorylation were upregulated in LPS-induced HK-2. Methyl jasmonate attenuated LPS-induced decrease of I kappa B alpha and increase of p65 and I kappa B alpha phosphorylation in HK-2 cell.Conclusion: Methyl jasmonate demonstrated anti-apoptotic and anti-inflammatory effects on LPS-induced HK-2 cell through suppression of NF-kappa B activation.