| Literature DB >> 30200740 |
Fu-Qun Liu1, Qi Gao2, Dan-Dan Wang2, Zhi-Xiong Zhang1.
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-1β and TNF-α was determined by ELISA. Western blot was performed to observe the protein expression of NLRP3, ASC, caspase-1 and IL-1β 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. Copyright© by the Chinese Pharmaceutical Association.Entities:
Keywords: Ginkgo biloba extract 50(GBE50) ; NLRP3 inflammasome ; adenosine triphosphate ; lipopolysaccharide ; microglia
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Year: 2018 PMID: 30200740 DOI: 10.19540/j.cnki.cjcmm.20180504.001
Source DB: PubMed Journal: Zhongguo Zhong Yao Za Zhi ISSN: 1001-5302