Handa Osamu, Yoshida Norimasa, Tanaka Yukiko, Ueda Miho, Ishikawa Takeshi, Takagi Tomohisa, Matsumoto Naoyuki, Naito Yuji, Yoshikawa Toshikazu
Department of Intrernal Medicine, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Can J Gastroenterol. 2002 Nov;16(11):785-9. doi: 10.1155/2002/631070.
Helicobacter pylori-infected gastrointestinal mucosa is frequently infiltrated by polymorphonuclear leukocytes (PMN) and monocytes, and these invading cells have been implicated in gastrointestinal mucosal inflammation. To clarify the efficacy of polaprezinc, a chelate compound consisting of zinc and L-carnosine, against H pylori-induced inflammation including PMN infiltration, the in vitro effects of this drug on interleukin (IL)-8 production by an established gastric cancer cell line (MKN 45 cells) and on PMN-endothelial cell adhesive interactions was investigated. Polaprezinc and zinc sulphate inhibited IL-8 production by MKN 45 cells in response to stimulation with H pylori water extract (HPE) in a dose-dependent manner from 10(-7) M to 10(-5) M. In addition, the expression of CD11b and CD18 on PMN and PMN-dependent adhesion to endothelial cells elicited by HPE was inhibited by polaprezinc and zinc sulphate in a concentration-dependent manner. L-carnosine did not have any effects on IL-8 production or PMN-endothelial cell interactions. These results suggest that polaprezinc, mainly the zinc component, may inhibit H pylori-induced PMN-mediated gastric inflammation by attenuating CD11b/CD18 expression on PMN and IL-8 production from gastric epithelial cells.
幽门螺杆菌感染的胃肠道黏膜常被多形核白细胞（PMN）和单核细胞浸润，这些侵入细胞与胃肠道黏膜炎症有关。为阐明聚普瑞锌（一种由锌和L-肌肽组成的螯合物）对幽门螺杆菌诱导的包括PMN浸润在内的炎症的疗效，研究了该药物对已建立的胃癌细胞系（MKN 45细胞）白细胞介素（IL）-8产生以及PMN与内皮细胞黏附相互作用的体外影响。聚普瑞锌和硫酸锌以剂量依赖方式（从10⁻⁷M至10⁻⁵M）抑制MKN 45细胞对幽门螺杆菌水提取物（HPE）刺激的IL-8产生。此外，聚普瑞锌和硫酸锌以浓度依赖方式抑制HPE诱导的PMN上CD11b和CD18的表达以及PMN对内皮细胞的依赖性黏附。L-肌肽对IL-8产生或PMN与内皮细胞的相互作用没有任何影响。这些结果表明，聚普瑞锌，主要是锌成分，可能通过减弱PMN上CD11b/CD18的表达和胃上皮细胞IL-8的产生来抑制幽门螺杆菌诱导的PMN介导的胃炎症。
