Sophoridine inhibits NF-kappaB signaling pathway activation in kidney tissue of endotoxemia mice / 药学学报
Acta Pharmaceutica Sinica
; (12): 1072-1077, 2011.
Article
in Zh
| WPRIM
| ID: wpr-233033
Responsible library:
WPRO
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.
Full text:
1
Index:
WPRIM
Main subject:
Pharmacology
/
Phosphorylation
/
Quinolizines
/
Blood
/
RNA, Messenger
/
Antitoxins
/
Signal Transduction
/
Random Allocation
/
Lipopolysaccharides
/
Tumor Necrosis Factor-alpha
Type of study:
Prognostic_studies
Limits:
Animals
Language:
Zh
Journal:
Acta Pharmaceutica Sinica
Year:
2011
Type:
Article