期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 124, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.intimp.2023.110902
关键词
Gastric precancerous lesions; Epithelial-mesenchymal transition; Tanshinone I; p38/STAT3; Gastric cancer
This study demonstrated that Tan-I inhibits the progression of gastric precancerous lesions by reversing the epithelial-mesenchymal transition process and reducing inflammation through the p38/STAT3 signaling pathway.
Background: Gastric precancerous lesions (GPLs) are omens for gastric cancer (GC), which developing with a series of pathological changes of gastric mucosa. Reversing epithelial-mesenchymal transition (EMT) in gastric mucosa is the main approach to restrain GPLs from evolving into cancer. Tanshinone I (Tan-I), the active ingredients of traditional Chinese herb Salvia miltiorrhiza, has exhibited anticancer effect. Purpose: To investigate the effect and mechanism of Tan-I in intervening GPLs, and provide a new therapeutic strategy for prevention of GC. Methods: Gastric mucosal epithelial cells were treated with the N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) to construct MNNG-induced cell (MC cell) of gastric mucosa that undergoing EMT process. Then, this study explored the effect and mechanism of Tan-I in vitro. Subsequently, this study constructed GPL mice to clarify the exact efficacy and mechanism of Tan-I on GPLs. Results: Tan-I inhibited MC cell proliferation, invasion and migration. Simultaneously, the aberrant expression of E-cadherin and N-cadherin were reversed. Tan-I attenuated inflammation by reducing the release of nitric oxide, TNF alpha and IL-1 beta. Tan-I reversed the EMT and inflammatory processes by regulating p38 and STAT3. Conclusion: This study showed that Tan-I inhibited the progression of GPLs by reversing the EMT process and reducing inflammation by restraining the p38/STAT3 signaling pathway.
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