首页|癸基泛醌对中波紫外线诱导的HaCaT细胞光损伤的作用及其机制

癸基泛醌对中波紫外线诱导的HaCaT细胞光损伤的作用及其机制

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目的:探讨癸基泛醌(DUb)对中波紫外线(UVB)诱导人永生化表皮角质细胞(HaCaT)光损伤的作用及其机制。方法:采用UVB辐射HaCaT细胞建立光损伤模型,设置对照组、UVB模型组(30 mJ/cm2 UVB)、UVB+低、中、高剂量(2。5、5和10 µmol/L)DUb干预组及DUb(10 µmol/L)组,共计6组。CCK-8法检测细胞活力;倒置显微镜下观察HaCaT细胞形态学改变;DCFH-DA荧光探针检测细胞内活性氧(ROS)含量;试剂盒检测超氧化物歧化酶(SOD)和还原型谷胱甘肽(GSH)及丙二醛(MDA)水平;流式细胞仪检测细胞凋亡率;Western blot检测细胞内Bax、Bcl-2、caspase-3及p53蛋白的表达。结果:与对照组比较,UVB模型组细胞活力显著降低(P<0。01),形态改变明显,ROS和MDA含量显著升高(P<0。01),GSH含量和SOD活性显著降低(P<0。01),细胞凋亡率增加(P<0。01)。DUb干预后显著提高了经UVB诱导的HaCaT细胞活力(P<0。05或P<0。01),减少细胞内ROS和MDA的生成(P<0。05,P<0。01),增加GSH含量和SOD活性(P<0。05或P<0。01),减少了细胞凋亡(P<0。01)。同时中、高剂量DUb干预组中促凋亡蛋白Bax、caspase-3及p53的水平显著低于UVB组(P<0。01),而抗凋亡蛋白Bcl-2的水平显著高于UVB组(P<0。01)。结论:DUb可以减轻UVB对HaCaT细胞的损伤,减少细胞的凋亡和增强细胞的抗氧化性。
Effect of decylubiquinone on UVB-induced photodamage in HaCaT cells and its mechanism
AIM:To investigate the protective effect of decylubiquinone(DUb)against medium-wave ultravio-let(UVB)-induced photodamage in HaCaT cells and its molecular mechanism.METHODS:The photodamage model was established by irradiating HaCaT cells with UVB.The experiment was divided into 6 groups:control group,UVB model group(30 mJ/cm2),UVB+low-,medium-and high-concentration(2.5,5 and 10 µmol/L)DUb groups,and DUb(10 µmol/L)group.Cell viability was detected using the CCK-8 assay.The morphological changes of the HaCaT cells were observed under a light microscope.The production of reactive oxygen species(ROS)content in the HaCaT cells was analyzed by fluorescence probe of DCFH-DA,and the superoxide dismutase(SOD)activity,intracellular glutathione(GSH)and malondialdehyde(MDA)levels were detected using biochemical reagents.The apoptosis rate was detected through flow cytometry.The protein expression levels of Bax、Bcl-2、caspase-3 and p53 were detected by Western blot.RESULTS:Compared with the control group,the cell viability of UVB model group was significantly decreased(P<0.01),and obvious morphological changes,ROS and MDA were significantly increased(P<0.01),GSH and SOD were significantly decreased(P<0.01),the apoptosis rate was increased(P<0.01).DUb pretreatment significantly increased the viability of UVB-induced photodamage HaCaT cells(P<0.01),decreased intracellular ROS and MDA production(P<0.05,P<0.01),increased GSH content and SOD activity(P<0.05,P<0.01),and reduced apoptosis(P<0.01).Addi-tionally,the protein expression levels of Bax,caspase-3 and p53 in medium-and high-dose DUb groups were significantly decreased(P<0.01),while the anti-apoptotic protein Bcl-2 was significantly increased(P<0.01).CONCLUSION:Dec-ylubiquinone can alleviate UVB-induced photodamage to HaCaT cells,reduce apoptosis and enhance the antioxidant ca-pacity of cells,and protect HaCaT cells against UVB radiation.

decylubiquinoneultraviolet BHaCaT cellsoxidative stressapoptosis

王妍、赵波、童嘉玲、马宇昕、王欣、亓翠玲、唐佩

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广东药科大学基础医学院,广东 广州 510006

暨南大学附属第一医院康复科,广东 广州 510632

癸基泛醌 中波紫外线 HaCaT细胞 氧化应激 细胞凋亡

2024

中国病理生理杂志
中国病理生理学会

中国病理生理杂志

CSTPCD北大核心
影响因子:1.065
ISSN:1000-4718
年,卷(期):2024.40(12)