Study on anti-inflammatory effect and underlying mechanism of DMY in LPS-induced septic mice
10.3969/j.issn.1000-484X.2016.04.003
- VernacularTitle:二氢杨梅素抗感染性休克的作用与机制研究
- Author:
Rui WANG
;
Juan LIU
;
Xiaohui SU
;
Jianyu CHEN
;
Fen YANG
;
Ting LI
- Publication Type:Journal Article
- Keywords:
Dihydromyricetin;
RAW264.7;
MAPK;
Lipopolysaccharide
- From:
Chinese Journal of Immunology
2016;32(4):465-469
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of dihydromyricetin (DMY) on LPS-induced septic shock in mice and the related underlying mechanism.Methods:The LPS-induced septic shock mice model was established after the mice were pre-treated by DMY for 7 days.The mortality rate was calculated at 24,48,72,96,120,144 and 168 h after the mice were intraperitoneal injected with LPS.For elucidation of underlying mechanism ,RAW246.7 were pre-incubated with DMY for 1 h,and then stimulated by LPS 100 ng/ml.Western blot was performed for determination of P-ERK,P-JNK and P-p38 expression.Immunohistochemistry was applied to explore c-Fos and c-Jun nucleus translocation.Results:DMY could significantly inhibit LPS-induced mice mortality.Inhibitory effect of DMY on the phosphorylation of JNK and p 38 contributed to the anti-inflammatory effect of DMY in vivo.Furthermore , DMY obviously prevented c-Fos and c-Jun nucleus translocation.Conclusion:The anti-inflammatory effect of DMY is attributed to the suppression on c-Fos and c-Jun nucleus translocation ,via inhibition of the phosphorylation of JNK and p 38.
