The drug resistance of tumor cells greatly reduces the efficacy of chemotherapy drugs in gastric cancer. Salvianolic acid B (Sal-B) is considered as a chemopreventive agent which suppresses oxidative stress and apoptosis. Therefore, the study aims to clarify the mechanism of Sal-B in drug-resistant gastric cancer cells. CCK8 assay analyzed cell viabilities after GES1, AGS and AGS/DDP cells were respectively treated by Sal-B of different concentration or after AGS/DDP cells were disposed by cisplatin (DDP) in different concentration. The colony formation, ROS generation, apoptosis, migration, invasion and EMT marker proteins were respectively analyzed through formation assay, ROS kits, TUNNEL staining, Wound healing, Transwell assays and Western blot. The results demonstrated that Sal-B acted alone or in synergy with DDP to reduce cell viabilities, initiate ROS generation, promote cell apoptosis, as well as decrease migration, invasion and EMT in AGS and AGS/DDP cells. AKT activator and mTOR activator significantly reversed the above effects of Sal-B. Collectively, Sal-B regulated proliferation, EMT and apoptosis to reduce the resistance to DDP via AKT/mTOR pathway in DDP-resistant gastric cancer cells. Sal-B could be a potential anti-drug resistance agent to chemotherapy in gastric cancer.

肿瘤细胞的耐药性大大降低了化疗药物对胃癌的疗效。Salvianolic acid B (Sal-B) 被认为是一种化学预防剂，可抑制氧化应激和细胞凋亡。因此，本研究旨在阐明Sal-B在耐药胃癌细胞中的作用机制。CCK8分析分析了GES1、AGS和AGS/DDP细胞分别用不同浓度的Sal-B处理或AGS/DDP细胞用不同浓度的顺铂(DDP)处理后的细胞活力。分别通过形成试验、ROS试剂盒、TUNNEL染色、伤口愈合、Transwell试验和Western印迹分析集落形成、ROS产生、细胞凋亡、迁移、侵袭和EMT标记蛋白。结果表明，Sal-B 单独或与 DDP 协同作用以降低细胞活力，启动 ROS 生成，促进细胞凋亡，以及减少 AGS 和 AGS/DDP 细胞中的迁移、侵袭和 EMT。AKT 激活剂和 mTOR 激活剂显着逆转了 Sal-B 的上述作用。总的来说，Sal-B 通过 AKT/mTOR 通路调节 DDP 抗性胃癌细胞的增殖、EMT 和细胞凋亡以降低对 DDP 的抗性。Sal-B 可能是胃癌化疗的潜在抗药性药物。