In vitro anti-inflammatory effect of apigenin in the Helicobacter pylori-infected gastric adenocarcinoma cells

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• 作者：Yuan-Chuen Wang ; ^{ycwang@nchu.edu.tw} ; Kai-Ming Huang
• 关键词：AP-1 ; activator protein 1 ; CagA ; cytotoxin associated antigen ; COX-2 ; cyclooxygenase-2 ; ERK1/2 ; extracellular signal regulated kinase 1/2 ; EtBr ; ethidium bromide ; H2DCF-DA ; dihydrodichlorofluorescein diacetate ; HE ; dihydroethidium ; ICAM-1 ; intercellular a
• 刊名：Food and Chemical Toxicology
• 出版年：2013
• 出版时间：March, 2013
• 年：2013
• 卷：53
• 期：Complete
• 页码：376-383
• 全文大小：1170 K

文摘

Infection with Helicobacter pylori causes extensive gastric epithelial cell inflammation which may progress to atrophic gastritis, intestinal metaplasia, and even gastric adenocarcinoma. Apigenin (4¡ä,5,7-Trihydroxyflavone) is widely distributed in fruits and vegetables, and is a well-known antiinflammatory supplement with low cytotoxicity. In this study, we investigated the anti-inflammatory effects of apigenin in H. pylori-infected MKN45 cells, for which I¦ÊB¦Á, cyclooxygenase-2 (COX-2), intercellular adhesion molecule-1 (ICAM-1), reactive oxygen species (ROS), interleukin-8 (IL-8), IL-6, IL-1¦Â, and mucin-2 (MUC-2) expressions were examined. Apigenin treatments (9.3-74 ¦ÌM) significantly increased the I¦ÊB¦Á expression, and thus inhibited nuclear factor kappa B (NF-¦ÊB) activation, and the inflammatory factor (COX-2, ICAM-1, ROS, IL-6, and IL-8) expressions decreased. The ROS levels decreased partially based on the intrinsic scavenging property of apigenin. In summary, apigenin treatments effectively inhibited NF-¦ÊB activation and the related inflammatory factor expressions, as well as increased MUC-2 expression in the H. pylori-infected MKN45 cells. The compound shows great potential as a candidate agent for the inhibition of H. pylori-induced extensive gastric epithelial cell inflammation.