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.
Highlights
Inflammation is the first response occurring after damage or infection, which was regulated by many inflammatory mediators, including cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and proinflammatory cytokines (IL-1β, IL-6, and TNF-α) [1,2,3]
It has been generally accepted that the excessive production of proinflammatory cytokines and mediators due to monocytes and macrophages activation plays an important role in the progression of many inflammatory disease, such as rheumatic arthritis, chronic bronchitis, colitis, and glomerulonephritis [4]
Erefore, the secretion of 6-Keot-PGF1α can reflect the activity of COX-1. e pathological prostaglandins are produced by catalytic COX-2, represented by PGE2, so the secretion of PGE2 can reflect the activity of COX-2 [18]
Summary
Inflammation is the first response occurring after damage or infection, which was regulated by many inflammatory mediators, including cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and proinflammatory cytokines (IL-1β, IL-6, and TNF-α) [1,2,3]. Monocytes and macrophages are activated; they secrete massive proinflammatory cytokines to regulate immune responses. E 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. E 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 Conclusion. e 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
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
