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  

Effect of decylubiquinone on UVB-induced photodamage in HaCaT cells and its mechanism

作　　者：王妍 赵波 童嘉玲 马宇昕[1] 王欣 亓翠玲[1] 唐佩 WANG Yan;ZHAO Bo;TONG Jialing;Ma Yuxin;WANG Xin;QI Cuiling;TANG Pei(School of Basic Medical Sciences,Guangdong Pharmaceutical University,Guangzhou 510006,China;Department of Rehabilitation,the First Affiliated Hospital,Jinan University,Guangzhou 510632,China)

机构地区：[1]广东药科大学基础医学院,广东广州510006 [2]暨南大学附属第一医院康复科,广东广州510632

出　　处：《中国病理生理杂志》2024年第12期2312-2318,共7页Chinese Journal of Pathophysiology

基　　金：国家自然科学青年基金项目(No.82302827);广东省中医药局科研项目(No.20242048);广州市基础与应用基础项目(No.202201010299,No.202201010307);广州市基础与应用基础优秀博士“续航”项目(No.2025A04J5306)。

摘　　要：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/cm^(2)UVB)、UVB+低、中、高剂量(2.5、5和10μmol/L)DUb干预组及DUb(10μmol/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。AIM:To investigate the protective effect of decylubiquinone(DUb)against medium-wave ultraviolet(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/cm^(2)),UVB+low-,medium-and high-concentration(2.5,5 and 10μmol/L)DUb groups,and DUb(10μmol/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.

关 键 词：癸基泛醌 中波紫外线 HACAT细胞 氧化应激 细胞凋亡 

分 类 号：R363[医药卫生—病理学] R758.14[医药卫生—基础医学] R329.28