胃癌前病变（GPLs）是胃癌（GC）的预兆，其发展伴随胃黏膜的一系列病理变化。逆转胃黏膜上皮间质转化（EMT）是抑制GPLs发展为癌症的主要途径。丹参酮I（Tan-I），即中药丹参的主要成分之一，具有抗癌作用。为了研究Tan-I在干预GPLs中的作用和机制，并为胃癌的预防提供新的治疗策略。我们将胃黏膜上皮细胞处理成N-甲基-N'-硝基-N-亚硝基脲（MNNG）诱导的胃黏膜细胞（MC细胞），这些细胞经历EMT过程。然后，本研究在体外探索了Tan-I的作用和机制。随后，本研究构建了GPL小鼠模型，以阐明Tan-I对GPLs的确切有效性和机制。Tan-I抑制了MC细胞的增殖、侵袭和迁移。同时，Tan-I逆转了E-cadherin和N-cadherin的异常表达。Tan-I通过减少一氧化氮、TNFα和IL-1β的释放来减轻炎症反应。Tan-I通过调节p38和STAT3来逆转EMT和炎症过程。本研究表明，Tan-I通过逆转EMT过程和抑制p38/STAT3信号通路来抑制GPLs的进展。版权所有 © 2023 Elsevier B.V. 保留所有权利。

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.To investigate the effect and mechanism of Tan-I in intervening GPLs, and provide a new therapeutic strategy for prevention of GC.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.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, TNFα and IL-1β. Tan-I reversed the EMT and inflammatory processes by regulating p38 and STAT3.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.Copyright © 2023 Elsevier B.V. All rights reserved.