Liu Bin, Dong Jun, Wang Shasha, Yu Haining, Li Zhongchao, Sun Pengfei, Zhao Lei
School of Medicine, Shandong University, Jinan, Shandong 250012, P.R. China.
Department of Hepatobiliary Surgery, Shandong Cancer Hospital, Shandong University, Jinan, Shandong 250117, P.R. China.
Exp Ther Med. 2021 Jul;22(1):663. doi: 10.3892/etm.2021.10095. Epub 2021 Apr 22.
(HP) infection is one of the most frequent bacterial infections in humans and is associated with the pathogenesis of gastric motility disorders such as delayed gastric emptying (DGE). Although HP infection is considered to delay gastric emptying, there has been little research on the underlying mechanism. Gastric motility involves interactions among gastrointestinal hormones, smooth muscle, enteric and extrinsic autonomic nerves and interstitial cells of Cajal (ICCs), and ICCs play an important role in gastrointestinal motility. Mutation or loss of stem cell factor (SCF) expression is known to reduce the number of ICCs or alter the integrity of the ICC network, contributing to gastrointestinal dysmotility. The aim of the present study was to investigate whether a reduction in ICCs contributes to the DGE caused by HP. A mouse model of HP infection was established and gastric emptying was compared between HP-infected and uninfected mice using the bead method. In addition, ICC counts and SCF expression levels in gastric tissue were evaluated using immunohistochemistry and western blotting, respectively. The results revealed that gastric emptying was significantly slower, the number of ICCs in gastric tissue was significantly reduced and the protein level of SCF in gastric tissue was significantly decreased in HP-infected mice compared with uninfected mice. Therefore, it may be concluded that HP reduced the number of ICCs by decreasing the expression of SCF protein in gastric tissue, thereby causing DGE.
幽门螺杆菌（HP）感染是人类最常见的细菌感染之一，与胃动力障碍如胃排空延迟（DGE）的发病机制有关。尽管HP感染被认为会延迟胃排空，但关于其潜在机制的研究很少。胃动力涉及胃肠激素、平滑肌、肠内和外在自主神经以及 Cajal 间质细胞（ICC）之间的相互作用，而 ICC 在胃肠动力中起重要作用。已知干细胞因子（SCF）表达的突变或缺失会减少 ICC 的数量或改变 ICC 网络的完整性，导致胃肠动力障碍。本研究的目的是探讨 ICC 数量的减少是否导致 HP 引起的 DGE。建立了 HP 感染的小鼠模型，并使用珠子法比较了 HP 感染小鼠和未感染小鼠的胃排空情况。此外，分别使用免疫组织化学和蛋白质印迹法评估胃组织中的 ICC 计数和 SCF 表达水平。结果显示，与未感染小鼠相比，HP 感染小鼠的胃排空明显减慢，胃组织中的 ICC 数量显著减少，胃组织中 SCF 的蛋白质水平显著降低。因此，可以得出结论，HP 通过降低胃组织中 SCF 蛋白的表达来减少 ICC 的数量，从而导致 DGE。
