The gastroprotective effect of alpinia officinarum extract on indomethacin-induced topical injuries in RGM-1 Cells: Involvement of H+/K+-ATPase- and mitochondrial-mediated apoptosis
The gastroprotective effect of alpinia officinarum extract on indomethacin-induced topical injuries in RGM-1 Cells: Involvement of H+/K+-ATPase- and mitochondrial-mediated apoptosis
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高良姜提取物对吲哚美辛诱导的 RGM-1 细胞局部损伤的胃保护作用：参与 H /K -ATP 酶和线粒体介导的细胞凋亡
DOI：
10.4103/pm.pm_65_20
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发表时间：
2021-04
影响因子：
0.7
通讯作者：
Junqing Zhang
中科院分区：
文献类型：
--
作者：
Li Li;Jingwen Gong;Hailong Li;Mingyan Zhou;Yinfeng Tan;Junqing Zhang
背景：局部效应是非甾体抗炎药（NSAIDs）致胃损伤的重要机制。我们的前期研究表明高良姜提取物（AOE）可能对吲哚美辛（INDO）的局部效应具有一定的保护作用。本研究的目的是阐明A.对INDO诱导的胃粘膜局部损伤的保护作用。材料和方法：用0.5mMINDO对大鼠胃上皮细胞（RGM-1）产生局部作用。同时，分别加入AOE（2.5 μg/mL）和高良姜素（GAL）（0.05 mM），观察其保护作用。流式细胞术、倒置荧光显微镜、酶标仪检测细胞增殖、线粒体活力和线粒体介导的凋亡。Western blot法检测caspase-3蛋白的表达。结果如下：AOE和GAL对INDO损伤的RGM-1细胞具有明显的保护作用，其作用机制可能与促进细胞增殖、上调线粒体活力、抑制线粒体细胞色素c释放、抑制脂质过氧化和caspase-3活性、抑制H+/K+-ATP酶活性有关。结论：AOE和GAL的胃保护作用与抑制胃酸分泌和抑制胃黏膜细胞凋亡密切相关。这些结果为阐明黄芪胃保护作用的机制提供了新的认识。在治疗非甾体抗炎药引起的胃粘膜损伤方面具有良好的临床应用前景。
Background: Topical effects are essential mechanisms of nonsteroidal anti-inflammatory drugs (NSAIDs)-induced gastric damage. Our previous study showed that the extract of Alpinia officinarum (AOE) may have some protective effects against the topical effects of indomethacin (INDO). The aim of this study was to elucidate the protective effects and mechanisms of A. officinarum against INDO-induced topical injuries to gastric mucosa. Materials and Methods: 0.5 mM INDO was used to cause topical effects to rat gastric epithelial cells (RGM-1). Meanwhile, AOE (2.5 μg/mL) and galangin (GAL) (0.05 mM) were added, respectively, to explore their protective effects. The cell proliferation, mitochondrial viability, and mitochondrial-mediated apoptosis were assessed by flow cytometry, inverted fluorescence microscope, or microplate reader. Pro- and cleaved-caspase-3 were detected by Western blot method. Results: AOE and GAL could significantly protect INDO-damaged RGM-1 cells by promoting cell proliferation, upregulating mitochondrial viability, inhibiting mitochondrial cytochrome c release into cytoplasm, inhibiting lipid peroxidation and caspase-3 activity, and suppressing H+/K+-ATPase activity. Conclusion: The gastroprotective effects of AOE and GAL were closely associated with suppressing the gastric acid secretion and restraining mitochondrial-mediated apoptosis. These data provided new perceptions into interpreting the underlying mechanisms of gastroprotective effects of A. officinarum and showed a promising clinical use in treating gastric mucosal injury induced by NSAIDs.