1. The Anti-Inflammatory Effect of Smilax china L. Extract on LPS-Stimulated THP-1 via Downregulation of MAPK and NF-κB Signaling Pathway.
- Author
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Jiang, Siyi, Wei, Qiong, Ye, Xiaochuan, Luo, Dan, Zhang, Xiaoyan, Li, Zhenglei, You, Pengtao, Huang, Xianzhang, and Liu, Yanwen
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CYTOKINES , *INTERLEUKINS , *HERBAL medicine , *HIGH performance liquid chromatography , *CELL migration , *IN vivo studies , *INFLAMMATION , *MICROBIOLOGICAL assay , *WESTERN immunoblotting , *CELLULAR signal transduction , *CELL survival , *GENE expression , *SARSAPARILLA , *MASS spectrometry , *DNA-binding proteins , *ENZYME-linked immunosorbent assay , *DOSE-effect relationship in pharmacology , *MESSENGER RNA , *TUMOR necrosis factors , *PLANT extracts , *CELL lines , *INFLAMMATORY mediators , *POLYMERASE chain reaction , *MOLECULAR structure , *CHINESE medicine , *PHOSPHORYLATION - Abstract
Background. Traditional Chinese medicine Smilax is the rhizome of liliaceous plant Smilax china L., which is used to treat pelvic inflammatory disease and anxieties. Purpose. To investigate the mechanism of anti-inflammatory activity of the extract from Smilax china L. (ES). Methods. The components of ES were identified by UPLC-QTOF-MS/MS. The anti-inflammatory activities were evaluated in xylene-induced ear oedema and egg white-induced plantar swelling test. Cell viability was examined by CCK-8 assay. The inflammatory mediators, proinflammatory cytokines, and MAPK and NF-κB signals in LPS-stimulated THP-1 cells were determined using ELISA, real-time PCR, and Western blot, respectively. Results. 20 compounds of ES were confirmed by comparing with the reference substance. ES displayed more prominent anti-inflammatory activity than the positive control "Jin Gang Teng" capsule in the in vivo acute inflammatory model. ES suppressed the expression of PGE2 and 6-Keot-PGF1α, and the ratio of IC50 (COX-1)/IC50 (COX-2) of ES was 3.15, which indicated that ES could selectively inhibit COX-2. ES dose-dependently (12.5, 25, and 50 mg/L) decreased the production and mRNA levels of proinflammatory cytokines IL-1β, IL-6, and TNF-α. Furthermore, ES significantly decreased LPS-induced phosphorylation of p38, JNK, ERK1/2, and p65, inhibiting the expression of IKKα and the degradation of IκBα. Conclusion. The results suggested that ES could selectively inhibit the activity of COX-2, and the anti-inflammatory effect of ES was associated with the inhibition of IL-1β, IL-6, and TNF-α via negative regulation of MAPK and NF-κB signaling pathways in LPS-induced THP-1 cells. [ABSTRACT FROM AUTHOR]
- Published
- 2021
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