白藜芦醇对脂多糖诱导的 HT-29 细胞炎症模型中紧密连接蛋白和 Notch1 通路的影响,Inflammation

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白藜芦醇对脂多糖诱导的 HT-29 细胞炎症模型中紧密连接蛋白和 Notch1 通路的影响
Inflammation ( IF 4.5 ) Pub Date : 2022-06-15 , DOI: 10.1007/s10753-022-01704-2
Yihua Luo ₁ , Xueyan Yu ₁ , Peizhuang Zhao ₁ , Jun Huang ₁ , Xue Huang ₁

Affiliation

溃疡性结肠炎 (UC) 与肠上皮紧密连接蛋白的破坏密切相关。多项研究证实，白藜芦醇（RSV）是一种天然多酚类化合物，具有潜在的抗炎作用，可以调节紧密连接蛋白的表达。然而，RSV 调节肠上皮紧密连接蛋白表达的机制仍不清楚。因此，我们研究了 RSV 对脂多糖 (LPS) 诱导的 HT-29 炎症细胞模型中紧密连接蛋白的潜在影响，并探讨了其作用机制。首先，在 LPS 诱导的炎症 HT-29 细胞模型中，紧密连接蛋白 occludin、ZO-1 和 claudin-1 的下调表达通过与 RSV 孵育被逆转，伴随着肿瘤坏死因子α-转换酶（TACE）表达的降低。此外，通过 RSV 处理，Notch1 通路减弱，炎症因子 IL-6 和 TNF-α 的表达降低。其次，在 Jagged-1 与 RSV 联合使用以重新激活 Notch1 通路后，RSV 对 LPS 诱导的紧密连接蛋白 occludin、ZO-1 和 claudin-1 表达减少的保护作用以及炎症因子 IL-6 和 TNF-α 的水平被废除。这些结果表明 RSV 可能通过减弱 Notch1 通路来调节紧密连接蛋白的表达。通过 RSV 处理，Notch1 通路减弱，炎症因子 IL-6 和 TNF-α 的表达降低。其次，在 Jagged-1 与 RSV 联合使用以重新激活 Notch1 通路后，RSV 对 LPS 诱导的紧密连接蛋白 occludin、ZO-1 和 claudin-1 表达减少的保护作用以及炎症因子 IL-6 和 TNF-α 的水平被废除。这些结果表明 RSV 可能通过减弱 Notch1 通路来调节紧密连接蛋白的表达。通过 RSV 处理，Notch1 通路减弱，炎症因子 IL-6 和 TNF-α 的表达降低。其次，在 Jagged-1 与 RSV 联合使用以重新激活 Notch1 通路后，RSV 对 LPS 诱导的紧密连接蛋白 occludin、ZO-1 和 claudin-1 表达减少的保护作用以及炎症因子 IL-6 和 TNF-α 的水平被废除。这些结果表明 RSV 可能通过减弱 Notch1 通路来调节紧密连接蛋白的表达。和 claudin-1 以及炎症因子 IL-6 和 TNF-α 水平的降低被消除。这些结果表明 RSV 可能通过减弱 Notch1 通路来调节紧密连接蛋白的表达。和 claudin-1 以及炎症因子 IL-6 和 TNF-α 水平的降低被消除。这些结果表明 RSV 可能通过减弱 Notch1 通路来调节紧密连接蛋白的表达。

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Effects of Resveratrol on Tight Junction Proteins and the Notch1 Pathway in an HT-29 Cell Model of Inflammation Induced by Lipopolysaccharide

Ulcerative colitis (UC) is closely associated with disruption of intestinal epithelial tight junction proteins. A variety of studies have confirmed that resveratrol (RSV), a natural polyphenolic compound, has a potential anti-inflammatory effect and can regulate the expression of tight junction proteins. However, the mechanism by which RSV regulates the expression of tight junction proteins in the intestinal epithelium remains unclear. Therefore, we investigated the potential effect of RSV on tight junction proteins in an HT-29 cell model of inflammation induced by lipopolysaccharide (LPS) and explored its mechanism of action. First, the downregulated expression of the tight junction proteins occludin, ZO-1, and claudin-1 in the HT-29 cell model of inflammation induced by LPS was reversed by incubation with RSV, accompanied by a decrease in the expression of tumor necrosis factor α-converting enzyme (TACE). Additionally, the Notch1 pathway was attenuated and the expression of the inflammatory factors IL-6 and TNF-α was decreased by treatment with RSV. Second, after Jagged-1 was used in combination with RSV to reactivate the Notch1 pathway, the protective effects of RSV against the LPS-induced reductions in the expression of the tight junction proteins occludin, ZO-1, and claudin-1 and the decreases in the levels of the inflammatory factors IL-6 and TNF-α were abolished. These results suggest that RSV might regulate the expression of tight junction proteins by attenuating the Notch1 pathway.

更新日期：2022-06-16

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