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The Anti-Inflammatory Effect of Smilax china L. Extract on LPS-Stimulated THP-1 via Downregulation of MAPK and NF-κB Signaling Pathway
Author(s) -
Siyi Jiang,
Qiong Wei,
Xiaochuan Ye,
Dan Luo,
Xiaoyan Zhang,
Zhenglei Li,
Pengtao You,
Xianzhang Huang,
Liu Yan-wen
Publication year - 2021
Publication title -
evidence-based complementary and alternative medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.552
H-Index - 90
eISSN - 1741-4288
pISSN - 1741-427X
DOI - 10.1155/2021/9958808
Subject(s) - proinflammatory cytokine , thp1 cell line , p38 mitogen activated protein kinases , mapk/erk pathway , pharmacology , nf κb , western blot , iκbα , tumor necrosis factor alpha , downregulation and upregulation , viability assay , traditional medicine , medicine , chemistry , signal transduction , inflammation , apoptosis , immunology , biology , cell culture , biochemistry , gene , genetics
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- κ B 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 PGE 2 and 6-Keot-PGF 1 α , and the ratio of IC 50 (COX-1)/IC 50 (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-1 β , IL-6, and TNF- α . Furthermore, ES significantly decreased LPS-induced phosphorylation of p38, JNK, ERK1/2, and p65, inhibiting the expression of IKK α and the degradation of I κ B α .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-1 β , IL-6, and TNF- α via negative regulation of MAPK and NF- κ B signaling pathways in LPS-induced THP-1 cells.

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