Methylprednisolone attenuates lipopolysaccharide-induced Fractalkine expression in kidney of Lupus-prone MRL/lpr mice through the NF-kappaB pathway

• DOI: 10.1186/s12882-015-0145-y
• Publication Date: 2015-08-26T11:32:41Z
• Authors: Yanwu You; Yueqiu Qin; Xu Lin; Fafen Yang; Jun Li; Suren R. Sooranna; Liao Pinhu
• Keywords: Nephritis; Intraperitoneal injection; Nephrology

Fractalkine (FKN) is involved in the occurrence and development of human lupus nephritis. It known to be upregulated by lipopolysaccharide (LPS) as a stimulus vivo. MRL/lpr mice have been used an vivo model study Methylprednisolone (MP) widely clinical treatment progressive glomerular diseases such The aim this explore mechanism LPS induced FKN expression determine whether other molecular mechanisms contribute signaling pathway MP action mice.Forty-eight female at 12 weeks age were randomly distributed into six groups. Each group received various treatments for 8 receiving twice weekly intraperitoneal injections (1) (MP-treated mice), (2) SC-514 (SC-514-induced (3) normal saline single injection (LPS-induced (4) (LPS + (5) SC mice) (6) (control mice). One-way ANOVA was data analysis P value <0.05 considered statistically significantly.The NF-kappaB p65 mRNA detected qPCR. protein activation immunohistochemistry western blots respectively. kidney significantly increased mediated NF-κB increase phospho-p65. reduced proteinuria ameliorated renal damage mice. well inhibitor, SC-514, inhibited LPS-induced NF-kappaB.The results indicate that attenuates through pathway.