title: [Sophoridine inhibits NF-kappaB signaling pathway activation in kidney tissue of endotoxemia mice].
abstract: This study is to investigate the effects of sophoridine on NF-kappaB signaling pathway in kidney tissue of endotoxemia mice and the mechanism involved. BALB/c mice were challenged with lipopolysaccharide (LPS) caudal vein injection, then sophoridine was administered by intraperitoneal injection. Totally 50 mice were divided into 5 groups: control group, LPS model group, sophoridine treatment 12 mg x kg(-1) group, 6 mg x kg(-1) group and 3 mg x kg(-1) group. All animals were sacrificed at 6 hours after treatment. Kidney and blood samples were harvested. IKKbeta mRNA and TNF-alpha mRNA expression of renal tissue was measured by the reverse transcription polymerase chain reaction (RT-PCR), and phosphorylation IKKbeta protein (pIKKbeta) was detected by immunohistochemistry. NF-kappaB P65 protein expression and distribution of renal tissue were observed by Western blotting and immunofluorescence laser confocal microscopy. Serum TNF-alpha level was detected by radioimmunoassay. The results showed that the sophoridine significantly reduced the expression of IKKbeta mRNA and pIKKbeta protein, and inhibited the expression of NF-kappaB P65 protein and decreased the entry nuclear rate of NF-kappaB P65 in the renal tissue of endotoxemia mice. Thereby the renal TNF-alpha mRNA expression and serum TNF-alpha level were significantly reduced. These results suggest that sophoridine could inhibit inflammatory reaction induced by LPS through inhibiting activation of NF-kappaB signaling pathway.
authors: Department of Pathogenic Biology and Immunology, School of Basic Medical Sciences, Ningxia Medical University, Yinchuan 750004, China.
authors: Ling
authors: L
authors: Huang
authors: Jian-ning
authors: JN
authors: Xie
authors: Jin-ping
authors: JP
authors: Liang
authors: Yun-hong
authors: YH
authors: Li
authors: Ya
authors: Y
authors: Zhou
mesh_terms: D000470:Alkaloids / Q000494:pharmacology*; D000818:Animals; D000992:Antitoxins / Q000494:pharmacology; D019446:Endotoxemia / Q000097:blood / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism*; D005260:Female; D051550:I-kappa B Kinase / Q000235:genetics / Q000378:metabolism*; D007668:Kidney / Q000378:metabolism; D008070:Lipopolysaccharides; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010766:Phosphorylation; D011807:Quinolizines / Q000494:pharmacology*; D012333:RNA, Messenger / Q000378:metabolism; D011897:Random Allocation; D015398:Signal Transduction / Q000187:drug effects; D051996:Transcription Factor RelA / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000235:genetics / Q000378:metabolism*; D000093842:Matrines
chemical_list: D000470:Alkaloids; D000992:Antitoxins; D008070:Lipopolysaccharides; D011807:Quinolizines; D012333:RNA, Messenger; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D051550:I-kappa B Kinase; C496562:Ikbkb protein, mouse; D000093842:Matrines