Polaprezinc (PZ) plays a role in the protection of gastric mucosa and inhibiting Helicobacter pylori (H. pylori) growth in vitro. The objective of this study was to determine the protective effects of PZ on human gastric epithelial cells (GES-1) against H. pylori-induced damage, while also examining heat shock protein 70 (HSP70) as a potential underlying factor in this protection. Our findings revealed that PZ exerted bactericidal effects against H. pylori strains. We also observed that PZ mitigated the H. pylori-induced damage to GES-1 cells by increasing cell viability, reducing LDH release, and decreasing the secretion of pro-inflammatory factors such as MCP-1 and IL-6. Co-culturing PZ with GES-1 cells significantly up-regulated the GES-1 HSP70 expression in both a time and dose-dependent manner. Pre-incubating (for 12 h) or co-culturing (for 24 h) GES-1 cells with PZ reversed the down-regulation of HSP70 in GES-1 cells caused by H. pylori infection. However, when quercetin was used to inhibit the up-regulation of HSP70 in GES-1 cells, the protective effect of PZ on GES-1 cells was significantly reduced. Based on the results of this study, PZ exhibits a protective role on GES-1 cells against H. pylori injury, as well as a direct bactericidal effect on H. pylori. HSP70 is involved in the PZ-driven host cell protection against H. pylori injury. These findings provide insight into alternative strategies for H. pylori treatment.

聚普锌（PZ）在体外具有保护胃粘膜和抑制幽门螺杆菌（H. pylori ）生长的作用。本研究的目的是确定 PZ 对人胃上皮细胞 (GES-1) 对抗幽门螺杆菌引起的损伤的保护作用，同时还检查热休克蛋白 70 (HSP70) 作为这种保护的潜在潜在因素。我们的研究结果表明，PZ 对幽门螺杆菌菌株具有杀菌作用。我们还观察到，PZ通过增加细胞活力、减少 LDH 释放和减少促炎因子（如 MCP-1 和 IL-6）的分泌来减轻幽门螺杆菌诱导的 GES-1 细胞损伤。PZ 与 GES-1 细胞共培养以时间和剂量依赖性方式显着上调 GES-1 HSP70 表达。将GES-1细胞与PZ预孵育（12小时）或共培养（24小时）逆转了幽门螺杆菌感染引起的GES-1细胞中HSP70的下调。然而，当槲皮素抑制GES-1细胞中HSP70的上调时，PZ对GES-1细胞的保护作用明显减弱。根据这项研究的结果，PZ对GES-1细胞表现出对幽门螺杆菌损伤的保护作用，并对幽门螺杆菌具有直接的杀菌作用。HSP70 参与 PZ 驱动的宿主细胞免受幽门螺杆菌损伤的保护。这些发现为幽门螺杆菌治疗的替代策略提供了见解。