Hu JiKe, Gao Lei, Maswikiti Ewetse Paul, Li Xuemei, Gu Baohong, Yu Yang, Li Haiyuan, Chen Hao
The Second Hospital and Clinical Medical School, Lanzhou University, Lanzhou, China.
Humanized Animal Model Laboratory of the Second Hospital of Lanzhou University, Lanzhou, China.
Sci Rep. 2025 Apr 7;15(1):11820. doi: 10.1038/s41598-025-96132-1.
In recent years, it has been discovered that the pathogenic effect of Helicobacter pylori (H. pylori) is not only limited to the gastroduodenal region, but also plays a certain role in the occurrence and development of liver diseases. The aim of this study is to ascertain the existence of Helicobacter pylori translocation, investigate whether it leads to liver injury and its potential mechanism and examine whether portal hypertension exacerbates liver damage caused by H. pylori translocation. Twenty four male SPF C57BL/6J mice were divided into four groups (6 in each group): (1) control group (Normal); (2) portal hypertension group (PHT); (3) H. pylori infected group (Hp); (4) H. pylori and Portal hypertension group (Hp and PHT). The histopathological changes of the liver and gastric tissues were measured by HE staining and immunohistochemistry (IHC); ALT, AST, IL-6 and INF-γ was measured by ELISA; Western blot detected the expression of pyroptotic proteins in the liver. The pro-inflammatory mediators and liver function indexes of mice in Hp group, Hp and PHT group were higher than those in the normal and PHT group. In addition, the liver inflammatory cell infiltration and ballooning of the two groups of mice were more severe than those in the normal group and PHT group, Hp and PHT group were more severe; Hp group, Hp and PHT group mice liver tissues activated the pyroptotic process through NLRP3 inflammasome, which eventually led to cell damage. Post mice infection by H. pylori, H. pylori will translocate to the liver, and induce liver injury by aggravating inflammation and promoting pyroptosis. Moreover, when portal hypertension occurs, it promotes the displacement of H. pylori, thereby aggravating liver injury.
近年来，人们发现幽门螺杆菌（H. pylori）的致病作用不仅局限于胃十二指肠区域，还在肝脏疾病的发生发展中发挥一定作用。本研究旨在确定幽门螺杆菌易位的存在，探讨其是否导致肝损伤及其潜在机制，并研究门静脉高压是否会加重幽门螺杆菌易位引起的肝损伤。将24只雄性SPF C57BL/6J小鼠分为四组（每组6只）：（1）对照组（正常组）；（2）门静脉高压组（PHT组）；（3）幽门螺杆菌感染组（Hp组）；（4）幽门螺杆菌与门静脉高压组（Hp和PHT组）。通过HE染色和免疫组织化学（IHC）检测肝脏和胃组织的组织病理学变化；采用ELISA法检测ALT、AST、IL-6和INF-γ；Western blot检测肝脏中焦亡蛋白的表达。Hp组、Hp和PHT组小鼠的促炎介质和肝功能指标高于正常组和PHT组。此外，两组小鼠肝脏炎症细胞浸润和气球样变比正常组和PHT组更严重，Hp和PHT组更甚；Hp组、Hp和PHT组小鼠肝脏组织通过NLRP3炎性小体激活焦亡过程，最终导致细胞损伤。小鼠感染幽门螺杆菌后，幽门螺杆菌会易位至肝脏，并通过加重炎症和促进焦亡诱导肝损伤。此外，当发生门静脉高压时，会促进幽门螺杆菌的移位，从而加重肝损伤。
