| 茹珂烨,阳东昊,张雨哲,等.羊栖菜硫酸多糖通过PI3K/AKT通路抑制H2O2诱导的MRC-5细胞氧化损伤[J].中国海洋药物,2023,42(6):21-28. |
| 羊栖菜硫酸多糖通过PI3K/AKT通路抑制H2O2诱导的MRC-5细胞氧化损伤 |
| The sulfated polysaccharide from Sargassum fusiforme protects MRC-5 cells against hydrogen peroxide ( H2O2 )-induced damage |
| 投稿时间：2022-09-15 修订日期：2022-12-07 |
| DOI：10.13400/j.cnki.cjmd.2023.06.023 |
| 中文关键词: 羊栖菜 硫酸多糖 MRC-5 细胞 PI3K / AKT/mTOR 信号通路 |
| English Keywords:Sargassum fusiforme sulfated polysaccharide MRC-5 cells PI3K/AKT/ mTOR pathway |
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| 中文摘要: |
| 目的 为阐明羊栖菜硫酸多糖(SFPS Ⅲ)对过氧化氢(H2O2)诱导的正常人胚肺细胞(MRC-5)氧化应激损伤的保护作用及潜在分子机制。方法 试验通过噻唑蓝(MTT)法检测MRC-5细胞暴露于H2O2或SFPS Ⅲ后的活力,Hoechst染色法检测细胞凋亡形态,流式细胞仪测定细胞凋亡率,酶联免疫吸附试验测定超氧化物歧化酶(SOD)和谷胱甘肽过氧化酶(GSH-Px)活性、一氧化氮(NO)和丙二醛(MDA)含量。通过免疫印迹Western blot检测相关蛋白水平。结果 H2O2处理使MRC-5细胞活力显著降低(P < 0.05),而SFPS Ⅲ(200～600 μg.mL-1)干预可明显增强MRC-5细胞活力。酶联免疫法结果表明,SFPS Ⅲ干预抑制H2O2诱导的细胞内NO和MDA的过度分泌,并增加了H2O2诱导的细胞内SOD和GSH-Px的活性。免疫印迹结果表明,120 μmol.L-1 H2O2处理的细胞中p-AKT和p-mTOR相对蛋白表达水平下调,而p-AKT和p-mTOR相对蛋白表达水平在SFPS Ⅲ处理的MRC-5细胞中被逆转。结论 SFPS Ⅲ对H2O2诱导的MRC-5细胞氧化应激损伤具有保护作用,其机制可能是激活PI3K/AKT/mTOR通路发挥其抗凋亡作用。研究结果为羊栖菜高附加值产品开发及天然、安全抗氧化功能因子的筛选提供了一定的理论依据。 |
| English Summary: |
| Objective The cytoprotective and potential molecular mechanisms of Sargassum fusiforme sulfated polysaccharide (SFPS Ⅲ) were investigated on the hydrogen peroxide (H2O2)-triggered damage in normal human embryonic lung (MRC-5) cells. Methods An MTT assay was conducted to assess the MRC-5 cell viability after exposure to H2O2 or SFPS Ⅲ. Apoptosis was detected by Hoechst staining. Cell apoptosis were explored via flow cytometry. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, nitric oxide (NO) release and malondialdehyde (MDA) levels were determined via enzyme-linked immunosorbent assay. The contents of related proteins were assessed via western blot. Results MRC-5 cells exhibited markedly decreased cellular viability after treatment with H2O2; however, treatment with SFPS Ⅲ (200-600 μg.mL-1) suppressed this decrease(P<0.05). Additionally, SFPS Ⅲ interference inhibited H2O2-induced overproduction of intracellular NO release and MDA levels and increased H2O2-induced intracellular SOD and GSH-Px activities. In these processes, the relative protein expression levels of phosphorylated (p)-AKT and p-mTOR were downregulated in 120 μmol.L-1 H2O2-treated cells compared with those of vehicle-treated cells. However, the relative expression levels of these proteins were reversed in SFPS Ⅲ-treated MRC-5 cells. Conclusion SFPS Ⅲ protected MRC-5 cells against H2O2-induced injury by activating the PI3K/AKT/mTOR pathway. The current study provides a theoretical basis for the developing of value-added products from Sargassum fusiforme and screening bioactive ingredients with safe antioxidant activity． |
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