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黄芩苷诱导自噬可防止 LPS 刺激的肠道细胞发生炎症和改变细胞旁通透性。

Baicalin-Induced Autophagy Preserved LPS-Stimulated Intestinal Cells from Inflammation and Alterations of Paracellular Permeability.

机构信息

Department of Biomedical and Dental Sciences and Morphofunctional Imaging, University of Messina, Polyclinic Hospital University, 98158 Messina, Italy.

出版信息

Int J Mol Sci. 2021 Feb 26;22(5):2315. doi: 10.3390/ijms22052315.

DOI:10.3390/ijms22052315
PMID:33652555
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7956379/
Abstract

Several studies have demonstrated a relevant role of intestinal epithelial cells in the immune response and in chronic inflammatory conditions, including ulcers, colitis, and Crohn's disease. Baicalin (BA), extracted from the root of Scutellaria baicalensis, has various beneficial healthy effects, including anti-inflammatory activity. However, few studies have evaluated BA effects on autophagic signaling in epithelial cell response to inflammatory stimuli. To explore possible beneficial effects of BA, HT-29 cells were exposed to lipopolysaccharide (LPS), in presence or absence of BA, for 4 h. We evaluated mRNA levels of autophagy-related genes and cytokines, triggering inflammatory response. Furthermore, the expression of claudin 1, involved in the regulation of paracellular permeability was analyzed. BA treatment repressed LPS-induced expression of TNF-α and IL-1β. The down-regulation of autophagy-related genes induced by LPS was counteracted by cell pretreatment with BA. Under these conditions, BA reduced the NF-κB activation caused by LPS. Also, BA restored mRNA and protein levels of claudin 1, which were reduced by LPS. In conclusion, in intestinal epithelial cells BA regulates the NF-κB activation and modulates both autophagic and inflammatory processes, leading to an improvement of paracellular permeability. These results suggest that the anti-inflammatory effects of BA can be associated to the regulation of autophagic flux.

摘要

已有多项研究表明,肠上皮细胞在免疫反应和慢性炎症状态(包括溃疡、结肠炎和克罗恩病)中发挥重要作用。黄芩苷(BA)是从黄芩的根部提取的,具有多种有益的健康作用,包括抗炎活性。然而,很少有研究评估 BA 对上皮细胞对炎症刺激的自噬信号的影响。为了探索 BA 的可能有益作用,将 HT-29 细胞暴露于脂多糖(LPS)中,存在或不存在 BA 的情况下孵育 4 小时。我们评估了自噬相关基因和细胞因子的 mRNA 水平,以触发炎症反应。此外,还分析了参与调节细胞旁通透性的 Claudin 1 的表达。BA 处理抑制了 LPS 诱导的 TNF-α和 IL-1β的表达。BA 预处理可逆转 LPS 诱导的自噬相关基因下调。在这些条件下,BA 降低了 LPS 引起的 NF-κB 激活。此外,BA 恢复了 LPS 降低的 Claudin 1 的 mRNA 和蛋白水平。总之,在肠上皮细胞中,BA 调节 NF-κB 的激活,并调节自噬和炎症过程,从而改善细胞旁通透性。这些结果表明,BA 的抗炎作用可能与自噬流的调节有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9325/7956379/e4d4b941c7fe/ijms-22-02315-g005.jpg
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