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Effect of Celastrus orbiculatus in inhibiting Helicobacter pylori induced inflammatory response by regulating epithelial mesenchymal transition and targeting miR-21/PDCD4 signaling pathway in gastric epithelial cells

Zhu, Yaodong, Liu, Lei, Hu, Lei, Dong, Wenqing, Zhang, Mei, Liu, Yanqing, Li, Ping
BMC complementary and alternative medicine 2019 v.19 no.1 pp. 91
Celastrus orbiculatus, Helicobacter pylori, Western blotting, alternative medicine, anti-inflammatory activity, antibacterial properties, antineoplastic activity, cytokines, enzyme-linked immunosorbent assay, epithelial cells, fluorescent antibody technique, gastric mucosa, gene expression, inflammation, messenger RNA, methylation, programmed cell death, quantitative polymerase chain reaction, reverse transcriptase polymerase chain reaction, secretion, signal transduction, toxicity testing, viability
BACKGROUND: The extract of Celastrus orbiculatus (COE) have been studied for anti-Helicobacter pylori (H. pylori) activity and anti-cancer effects in vitro and in vivo. However, the molecular mechanism by which COE inhibits H. pylori-induced inflammatory response has not been fully elucidated so far. METHODS: The effects of COE on viability, morphological changes, inflammatory cytokine secretion, protein and mRNA expression were analyzed by MTT assay, enzyme-linked immunosorbent assay (ELISA), immunofluorescence, western blot and real-time PCR (RT-PCR), respectively. The methylation level of programmed cell death 4 (PDCD4) promoter was investigated by methylation-specific PCR. (MSP) . RESULTS: COE effectively inhibited the H.pylori-induced inflammatory response by regulating epithelial-mesenchymal transition (EMT). The methylation level of PDCD4 promoter was suppressed by COE, which increased the expression ofPDCD4. Moreover, COE could inhibit microRNA-21 (miR-21) expression, as shown by an enhancement of its target gene PDCD4. Furthermore, both miR-21 over-expression and PDCD4 silencing attenuated the anti-inflammatory effect. of COE. CONCLUSIONS: COE inhibits H. pylori induced inflammatory response through regulating EMT, correlating with inhibition of miR-21/PDCD4 signal pathways in gastric epithelial cells.