This study aimed to elucidate the anti-inflammatory and antioxidant properties of resveratrol (RSV) in human gingival fibroblasts (HGFs) following stimulation by P. gingivalis lipopolysaccharide (LPS). The levels of the inflammatory cytokines IL-1β, IL-6, IL-8 and TNFα, the activity of the antioxidant enzymes SOD and GSH-Px, and the levels of MDA, were evaluated by ELISA. It was observed that the expression of IL-1β, IL-6, IL-8 and TNFα in LPS-induced HGFs was significantly downregulated by RSV in a dose-dependent manner. RSV also partly increased oxidative stress (OS)-related factors, including SOD and GSH-Px, which was accompanied by a decrease in MDA production, although the results were not statistically significant. Additionally, RSV-induced deactivation of the PI3K/AKT and Wnt/β-catenin pathways in LPS-induced HGFs was observed by western blot analysis. Subsequently, it was demonstrated treatment with PI3K/AKT pathway inhibitor (LY294002) or Wnt/β-catenin pathway inhibitor (Dickkopf-1, DKK-1) could further enhance the anti-inflammatory and antioxidant effects of RSV by downregulating the expression of IL-1β, IL-6, IL-8 and TNFα, and the production of MDA, and increasing the activity of SOD and GSH-Px in LPS-induced HGFs. These results suggested RSV attenuated the inflammation and OS injury of P. gingivalis LPS-treated HGFs by deactivating the PI3K/AKT and Wnt/β-catenin signaling pathways.

中文翻译：

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白藜芦醇通过靶向 PI3K/AKT 和 Wnt/β-catenin 信号通路防止 LPS 诱导的人牙龈成纤维细胞的炎症和氧化应激反应。

本研究旨在阐明白藜芦醇 (RSV) 在受牙龈脂多糖 (LPS) 刺激后在人牙龈成纤维细胞 (HGF) 中的抗炎和抗氧化特性。通过ELISA评估炎性细胞因子IL-1β、IL-6、IL-8和TNFα的水平，抗氧化酶SOD和GSH-Px的活性以及MDA的水平。观察到 LPS 诱导的 HGF 中 IL-1β、IL-6、IL-8 和 TNFα 的表达被 RSV 以剂量依赖性方式显着下调。RSV 还部分增加了氧化应激 (OS) 相关因素，包括 SOD 和 GSH-Px，这伴随着 MDA 产量的减少，尽管结果没有统计学意义。此外，通过蛋白质印迹分析观察到 RSV 诱导的 LPS 诱导的 HGF 中 PI3K/AKT 和 Wnt/β-连环蛋白途径的失活。随后，证明用 PI3K/AKT 通路抑制剂（LY294002）或 Wnt/β-catenin 通路抑制剂（Dickkopf-1、DKK-1）治疗可以通过下调 IL 的表达进一步增强 RSV 的抗炎和抗氧化作用-1β、IL-6、IL-8 和 TNFα，以及 MDA 的产生，并增加 LPS 诱导的 HGF 中 SOD 和 GSH-Px 的活性。这些结果表明 RSV 通过使 PI3K/AKT 和 Wnt/β-catenin 信号通路失活，减轻了牙龈卟啉单胞菌 LPS 处理的 HGF 的炎症和 OS 损伤。DKK-1)可通过下调IL-1β、IL-6、IL-8和TNFα的表达和MDA的产生，增加SOD和GSH的活性，进一步增强RSV的抗炎和抗氧化作用。 LPS 诱导的 HGF 中的 Px。这些结果表明 RSV 通过使 PI3K/AKT 和 Wnt/β-catenin 信号通路失活，减轻了牙龈卟啉单胞菌 LPS 处理的 HGF 的炎症和 OS 损伤。DKK-1)可通过下调IL-1β、IL-6、IL-8和TNFα的表达和MDA的产生，增加SOD和GSH的活性，进一步增强RSV的抗炎和抗氧化作用。 LPS 诱导的 HGF 中的 Px。这些结果表明 RSV 通过使 PI3K/AKT 和 Wnt/β-catenin 信号通路失活，减轻了牙龈卟啉单胞菌 LPS 处理的 HGF 的炎症和 OS 损伤。