梁梦迪,鲁芳,邹琪,等.海洋来源吲哚化合物对UVA致HaCaT细胞光老化损伤的保护作用[J].中国海洋药物,2026,(3):-.
海洋来源吲哚化合物对UVA致HaCaT细胞光老化损伤的保护作用
The Protective Effect of Marine-derived Indole on Photoaging Damage of HaCaT Cells Caused by UVA
投稿时间:2024-12-04  修订日期:2025-03-21
DOI:
中文关键词:  吲哚化合物  皮肤光老化  UVA  线粒体功能  抗氧化
English Keywords:indole compounds  skin photoaging  UVA  mitochondrial function  antioxidant
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作者单位邮编
梁梦迪 中国海洋大学 海洋药物教育部重点实验室 266003
鲁芳 中国海洋大学 海洋药物教育部重点实验室 
邹琪 中国海洋大学 海洋药物教育部重点实验室 
于艺薇 中国海洋大学 海洋药物教育部重点实验室 
张朋言 青岛海洋生物医药研究院 
杨文哲 青岛海洋生物医药研究院 
李海花 中国海洋大学 海洋药物教育部重点实验室 
郝杰杰* 中国海洋大学 海洋药物教育部重点实验室 266003
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中文摘要:
      探究吲哚化合物对长波紫外线(UVA)致皮肤光老化损伤的保护作用。方法 利用0.5 J/cm2 UVA诱导人永生化表皮细胞(HaCaT)建立光老化损伤模型,MTT法检测25、50、100、200、400、800 μmol/L吲哚对UVA辐照后HaCaT细胞增殖活力的影响;DCFH-DA荧光探针检测细胞内活性氧(ROS)含量;JC-1荧光探针检测线粒体膜电位(MMP)变化;还原型谷胱甘肽(GSH)和总抗氧化能力(T-AOC)检测抗氧化活性;免疫荧光法(IF)观察磷酸化组蛋白H2A.X(γ-H2A.X)检测DNA损伤水平;线粒体复合物活性及透射电镜(TEM)检测线粒体形态及功能;酶联免疫吸附试验(ELISA)检测细胞内炎性因子水平。结果 吲哚各浓度处理对细胞增殖活性均无显著影响;与UVA组相比,200 μmol/L吲哚处理后,HaCaT细胞增殖活性上升。进一步实验显示,与UVA组相比,吲哚组ROS含量下降,GSH、T-AOC活性上升,MMP回升,DNA损伤改善,线粒体复合物活性提高,促炎因子(IL-6)表达水平下降,抗炎因子(IL-37)表达水平上升。结论 吲哚可增强UVA辐照后HaCaT细胞的增殖活性及抗氧化水平,减少UVA产生的氧化应激损伤和炎性因子水平,保护线粒体功能,其潜在机制可能与线粒体相关。
English Summary:
      Objective To explore the protective effect of Indole compounds on skin photoaging damage caused by long-wave ultraviolet (UVA). Methods A photoaging damage model of human immortalized epidermal HaCaT cells was established using 0.5 J/cm2 UVA. The MTT assay was used to detect the effect of Indole of 25, 50, 100, 200, 400, 800 μmol/L on the viability of HaCaT cells after UVA irradiation; the DCFH-DA fluorescent probe for measuring intracellular reactive oxygen species (ROS) content; the JC-1 fluorescent probe for detecting changes in mitochondrial membrane potential (MMP); the detection of glutathione (GSH) and total antioxidant capacity (T-AOC) for examining antioxidant activities; Immunofluorescence to observe γ-H2A.X for detecting DNA damage level; the activities of mitochondrial complexes and transmission electron microscopy to detect the morphology and function of mitochondria and enzyme-linked immunosorbent assay (ELISA) to measure the levels of intracellular inflammatory factors. Results Various concentrations of Indole (25, 50, 100, 200, 400, 800 μmol·L?1) had no significant effect on cell viability. Compared with the UVA group, the viability of HaCaT cells increased after treatment with 200 μmol·L?1 of Indole. Further experiments showed that, compared with the UVA group, the Indole group had decreased ROS content, increased activities of GSH and T-AOC, recovered MMP, improved DNA damage, enhanced mitochondrial complex activity, the reduced expression level of the pro-inflammatory factor (IL-6), and increased expression level of the anti-inflammatory factor (IL-37). Conclusion Indole can enhance the proliferation and antioxidant level of HaCaT cells after UVA irradiation, mitigate UVA-induced oxidative stress and inflammatory factor levels, and protect mitochondrial function. Its potential mechanism may be related to mitochondria.
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