The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal epithelial cells injury
The protective effect of icariin and phosphorylated icariin against LPS-induced intestinal epithelial cells injury
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淫羊藿苷及磷酸化淫羊藿苷对LPS诱导的肠上皮细胞损伤的保护作用
DOI：
10.1016/j.biopha.2019.109246
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发表时间：
2019-10-01
影响因子：
7.5
通讯作者：
Wang, Zili
中科院分区：
文献类型：
--
作者：
Xiong, Wen;Ma, Haoyue;Wang, Zili
淫羊藿苷（ICA）和磷酸化淫羊藿苷（pICA）具有优异的抗病毒和抗氧化作用。然而，ICA 和 pICA 是否会引起抗 LPS 诱导的肠道损伤仍不清楚。在本研究中，我们以Caco-2细胞为模型，研究ICA和pICA对人结肠上皮细胞的保护作用并探讨其潜在机制。我们的结果表明 ICA 和 pICA 增加了 Caco-2 细胞中的细胞活力并降低了乳酸脱氢酶活性。 ICA 和 pICA 还减弱了 LPS 诱导的肠上皮细胞通透性变化，并降低了 Caco-2 细胞中氧化应激指标的水平，例如活性氧、丙二醛和过氧化氢。 ICA和pICA组的抗氧化指标，如超氧化物歧化酶、谷胱甘肽过氧化物酶、过氧化氢酶和总抗氧化能力升高，而IL-1β、IL-6、IL-8和TNF-α水平降低。此外，ICA和pICA降低了Caco-2细胞中caspase-3、-8、-9和-10的基因丰度和酶活性。我们的数据表明，ICA 和 pICA 有效减弱 LPS 诱导的肠上皮细胞氧化应激、炎症、细胞凋亡和肠道通透性的变化。这些发现为治疗脂多糖引起的肠道损伤提供了新的见解。
Icariin (ICA) and phosphorylated icariin (pICA) have excellent antiviral and antioxidant effects. However, whether ICA and pICA cause anti-LPS-induced intestinal damage remains unclear. In this study, we used Caco-2 cells as a model to investigate the protective effects of ICA and pICA on human colonic epithelial cells and explore their potential mechanisms. Our results indicated that ICA and pICA increased cell viability and decreased lactate dehydrogenase activity in Caco-2 cells. ICA and pICA also attenuated LPS-induced changes in intestinal epithelial cell permeability and reduced the levels of oxidative stress indicators, such as reactive oxygen species, malondialdehyde, and hydrogen peroxide, in Caco-2 cells. Antioxidant indicators, such as superoxide dismutase, glutathione peroxidase, catalase and total antioxidant capacity, were increased, while the levels of IL-1 beta, IL-6, IL-8 and TNF-alpha were reduced in the ICA and pICA groups. Furthermore, ICA and pICA decreased the gene abundance and enzyme activities of caspase-3, -8, -9 and -10 in Caco-2 cells. Our data suggest that ICA and pICA effectively attenuated LPS-induced changes in the oxidative stress, inflammation, apoptosis and intestinal permeability of intestinal epithelial cells. These findings provide new insight for treating LPS-induced intestinal injury.