Inhibition of lipopolysaccharide-induced inflammation in RAW264.7 macrophages by sinomenine through regulating heme oxygenase-1 expression and autophagy.
10.11817/j.issn.1672-7347.2018.09.006
- Author:
Yue PENG
1
;
Hao OU
1
;
Mingshi YANG
1
;
Yu JIANG
2
,
3
;
Min GAO
1
Author Information
1. Department of Critical Care Medicine, Third Xiangya Hospital, Central South University, Changsha 410013, China.
2. Institute of Emergency Medicine
3. Hunan Provincial Key Laboratory of Emergency and Critical Care Metabonomics, Hunan Provincial People's Hospital, Changsha 410005, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Anti-Inflammatory Agents;
pharmacology;
Autophagy;
drug effects;
Gene Expression Regulation, Enzymologic;
drug effects;
Heme Oxygenase-1;
genetics;
Inflammation;
chemically induced;
Lipopolysaccharides;
Macrophages;
drug effects;
Mice;
Morphinans;
pharmacology
- From:
Journal of Central South University(Medical Sciences)
2018;43(9):964-970
- CountryChina
- Language:Chinese
-
Abstract:
To investigate the effect of sinomenine on lipopolysaccharide (LPS)-induced inflammation in RAW264.7 macrophages and the underlying mechanisms.
Methods: The mouse RAW264.7 macrophages were treated with sinomenine and/or LPS with or without heme oxygenase-1 (HO-1) inhibitor Znpp. Real-time PCR, ELISA, immunofluenscence, and Western blot were used to detect the mRNA expression of TNF-α and IL-6, the release of TNF-α and IL-6, the protein expression of HO-1 and autophagy, respectively.
Results: Compared with the control group, the mRNA expression and release of inflammatory cytokines TNF-α and IL-6 were increased, the green fluorescence of autophagy-related protein LC3 was accumulated and the protein expression of HO-1 was increased in RAW264.7 cells after LPS treatment (P<0.05). Compared with the LPS group, sinomenine treatment could reduce the mRNA expression and release of TNF-α and IL-6, accompanied by increasess in green fluorescence aggregation of LC3 and HO-1 production (P<0.05). HO-1 inhibitor Znpp could weaken the ability of sinomenine through suppressing TNF-α and IL-6 expression and decreasing the aggregation of LC3 green fluorescence (P<0.05).
Conclusion: Sinomenine could alleviate LPS-induced inflammation in RAW264.7 macrophages, which might be related to HO-1 mediated autophagy. This study provides an experimental and theoretical basis for the clinical application of sinomenine in prevention and treatment of inflammation.
