Effects of GBE50 on LPS/ATP induced NLRP3 inflammasome activation in primary rat microglia.
10.19540/j.cnki.cjcmm.20180504.001
- Author:
Fu-Qun LIU
1
;
Qi GAO
2
;
Dan-Dan WANG
2
;
Zhi-Xiong ZHANG
1
Author Information
1. Department of Physiology in School of Basic Medicine， Shanghai University of Traditional Chinese Medicine， Shanghai 201203, China.
2. Shanghai Xingling Sci. & Tech. Pharmaceutical Co.， Ltd.， Shanghai 210703, China.
- Publication Type:Journal Article
- Keywords:
Ginkgo biloba extract 50(GBE50);
NLRP3 inflammasome;
adenosine triphosphate;
lipopolysaccharide;
microglia
- From:
China Journal of Chinese Materia Medica
2018;43(16):3346-3352
- CountryChina
- Language:Chinese
-
Abstract:
In this study, the anti-inflammatory mechanism of Ginkgo biloba extract 50 (GBE50) and its mechanism of action on NLRP3 inflammatory corpuscles were observed by primary microglia cells. LPS/ATP was used to stimulate microglia, and the best time for stimulation and optimal concentration of GBE50 were screened. Pro-inflammatory cytokine IL-1 and TNF-α was determined by ELISA. Western blot was performed to observe the protein expression of NLRP3, ASC, caspase-1 and IL-1 in cultured primary rat microglia. Effect of GBE50 on NLRP3 inflammatory corpuscle aggregation was detected by CO-IP. GBE50 (10 mg·L⁻¹) preconditioning could significantly inhibit the expression of LPS (100 μg·L⁻¹,12 h), ATP (5 mmol·L⁻¹, 30 min) induced primary microglia corpuscle associated protein, inflammatory corpuscle aggregation, and the release of inflammatory factors IL-6 and TNF-α. These results indicated that GBE50 could inhibit the secretion of inflammatory factors after microglia activation, which is related to down regulating the protein expression and activity of NLRP3 inflammatory corpuscle.
