Heat shock protein 70 is involved in polaprezinc driven cell protection against Helicobacter pylori-induced injury

IF 4.5 3区医学 Q1 MICROBIOLOGY

International Journal of Medical Microbiology Pub Date : 2023-05-01 DOI:10.1016/j.ijmm.2023.151582

Fansen Meng , Siying Zhu , Meiliang Gong , Hongjin Tao , Weihua Wang , Gangshi Wang

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引用次数: 0

Abstract

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.

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热休克蛋白70参与了polaprezinc驱动的细胞对幽门螺杆菌诱导的损伤的保护

吡嗪酮（PZ）在体外具有保护胃黏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）对幽门螺杆菌诱导的损伤的保护作用，同时检测热休克蛋白70（HSP70）作为这种保护的潜在潜在潜在因素。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，减轻了幽门螺杆菌诱导的GES-1细胞损伤。PZ与GES-1细胞共培养以时间和剂量依赖的方式显著上调GES-1 HSP70的表达。预孵育（12小时）或与PZ共培养（24小时）GES-1细胞逆转了幽门螺杆菌感染引起的GES-1中HSP70的下调。然而，当槲皮素用于抑制GES-1细胞中HSP70的上调时，PZ对GES-1的保护作用显著降低。根据本研究的结果，PZ对GES-1细胞对幽门螺杆菌损伤具有保护作用，并对幽门螺杆杆菌具有直接杀菌作用。HSP70参与PZ驱动的宿主细胞对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。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

International Journal of Medical Microbiology 医学-病毒学

CiteScore

9.70

自引率

0.00%

发文量

审稿时长

45 days

期刊介绍： Pathogen genome sequencing projects have provided a wealth of data that need to be set in context to pathogenicity and the outcome of infections. In addition, the interplay between a pathogen and its host cell has become increasingly important to understand and interfere with diseases caused by microbial pathogens. IJMM meets these needs by focussing on genome and proteome analyses, studies dealing with the molecular mechanisms of pathogenicity and the evolution of pathogenic agents, the interactions between pathogens and host cells ("cellular microbiology"), and molecular epidemiology. To help the reader keeping up with the rapidly evolving new findings in the field of medical microbiology, IJMM publishes original articles, case studies and topical, state-of-the-art mini-reviews in a well balanced fashion. All articles are strictly peer-reviewed. Important topics are reinforced by 2 special issues per year dedicated to a particular theme. Finally, at irregular intervals, current opinions on recent or future developments in medical microbiology are presented in an editorial section.