Mechanism of curcumin on improving cell damage induced by ultraviolet B irradiation
- JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY Vol. 34, Issue 9, Pages: 753-758(2025)
- 作者机构：
首都医科大学附属北京安贞医院南充医院•南充市中心医院 皮肤科，四川 南充 637000
- 作者简介：
- 基金信息：
DOI：10.11659/jjssx.01E025076
CLC： R758.1;R965Received：14 January 2025，
Published：25 September 2025
- 稿件说明：
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陈颖,赵菊花,杨羽等.姜黄素改善中波紫外线照射细胞损伤的机制研究[J].局解手术学杂志,2025,34(09):753-758.
CHEN Ying,ZHAO Ju-hua,YANG Yu,et al.Mechanism of curcumin on improving cell damage induced by ultraviolet B irradiation[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(09):753-758.
陈颖,赵菊花,杨羽等.姜黄素改善中波紫外线照射细胞损伤的机制研究[J].局解手术学杂志,2025,34(09):753-758. DOI： 10.11659/jjssx.01E025076.
CHEN Ying,ZHAO Ju-hua,YANG Yu,et al.Mechanism of curcumin on improving cell damage induced by ultraviolet B irradiation[J].JOURNAL OF REGIONAL ANATOMY AND OPERATIVE SURGERY,2025,34(09):753-758. DOI： 10.11659/jjssx.01E025076.
摘要
目的
2
探讨姜黄素（CUR）通过Toll样受体4（TLR4）/核因子-κB（NF-κB）/核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）信号通路对中波紫外线（UVB）诱导的角质形成细胞氧化损伤的影响。
方法
2
体外正常培养人角质形成细胞HaCaT，以57 mJ/cm
2
的UVB照射建立角质形成细胞氧化损伤模型，正常培养的细胞为Control组，建模后的细胞为UVB组，建模后经5 μmol/L CUR处理的细胞为CUR组，建模后经100 μg/L TLR4抑制剂TAK-242处理的细胞为TAK-242组，建模后经5 μmol/L CUR及100 nmol/L TLR4激活剂脂多糖（LPS）处理的细胞为CUR+LPS组。qRT-PCR检测各组细胞中TLR4、NF-κB、NLRP3 mRNA的表达水平；CCK-8检测各组细胞的增殖情况；根据试剂盒说明书采用荧光法检测各组细胞中活性氧（ROS）相对含量，超氧化物歧化酶（SOD）、过氧化氢酶（CAT）活力，丙二醛（MDA）、谷胱甘肽（GSH）浓度；ELISA检测各组细胞中肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）等炎症因子的表达水平；流式细胞仪检测各组细胞的凋亡水平；Western blot检测各组细胞中增殖相关蛋白增殖细胞核抗原（PCNA）、凋亡相关蛋白[B淋巴细胞瘤-2（Bcl-2）、Bcl-2相关X蛋白（Bax）
]
及TLR4/NF-κB/NLRP3信号通路相关蛋白（TLR4、NF-κB、NLRP3）表达。
结果
2
与Control组相比，UVB组细胞存活率，PCNA、Bcl-2蛋白表达水平，SOD、CA
T活力，GSH浓度降低，而细胞凋亡率，Bax蛋白水平，ROS相对含量，MDA浓度，TNF-α、IL-1β水平，TLR4、NF-κB、NLRP3 mRNA和蛋白水平升高（
P
<
0.05）；与UVB组相比，TAK-242组、CUR组细胞存活率，PCNA、Bcl-2蛋白表达水平，SOD、CAT活力，GSH浓度升高，而细胞凋亡率，Bax蛋白水平，ROS相对含量，MDA浓度，TNF-α、IL-1β水平，TLR4、NF-κB、NLRP3 mRNA和蛋白水平降低（
P
<
0.05）；与CUR组相比，CUR+LPS组细胞存活率，PCNA、Bcl-2蛋白表达水平，SOD、CAT活力，GSH浓度降低，而细胞凋亡率，Bax蛋白表达水平，ROS相对含量，MDA浓度，TNF-α、IL-1β水平，TLR4、NF-κB、NLRP3 mRNA和蛋白水平升高（
P
<
0.05）。
结论
2
CUR能够提高角质形成细胞的抗氧化应激水平，减轻炎症反应，促进细胞增殖，改善UVB照射引起的细胞损伤，其机制可能与抑制TLR4/NF-κB/NLRP3信号通路有关。
Abstract
Objective
2
To explore the effect of curcumin （CUR） on oxidative damage of keratinocytes induced by ultraviolet B （UVB） irradiation through Toll-like receptor 4 （TLR4）/nuclear factor-kappa B （NF-κB）/nucleotide-binding oligomerization domain-containing protein 3 （NLRP3）signaling pathway.
Methods
2
Human keratinocytes of HaCaT were cultured normally in vitro，and the keratinocyte oxidative damage model was established by the irradiation of 57 mJ/cm
2
UVB. The cells with normal culture were as the control group，the cells treated after modeling were as the UVB group，the cells treated with 5 μmol/L CUR after modeling were as the CUR group，the cells treated with 100 μg/L TLR4 inhibitor of TAK-242 after modeling were as the TAK-242 group，and the cells treated with 5 μmol/L CUR and 100 nmol/L TLR4 activator of lipopolysaccharide（LPS） were as the CUR+LPS group. qRT-PCR was applied to detect the relative expression levels of TLR4，NF-κB，and NLRP3 mRNAs of cells in each group. CCK-8 was applied to detect the cell proliferation in each group. The relative content of reactive oxygen species （ROS），the viabilities of superoxide dismutase （SOD） and catalase （CAT），and the concentrations of glutathione （MDA） and glutathione （GSH） of cells in each group were detected by fluorescence assay according to the kit instruction. ELISA kit was used to detect the expre
ssion of inflammatory factors of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） of cells in each group. Flow cytometry was applied to detect the cell apoptosis in each group. Western blot was applied to detect the expression of proliferation related protein of proliferating cell nuclear antigen （PCNA），apoptosis related proteins ［B-cell lymphoma-2（Bcl-2） and Bcl-2-associated X protein （Bax）］，and TLR4/NF-κB/NLRP3 signaling pathway related proteins （TLR4，NF-κB and NLRP3） of cells in each group.
Results
2
Compared with the Control group，the cell survival rate，the expression levels of PCNA and Bcl-2 proteins，the viabilities of SOD and CAT，and the GSH concentration in the UVB group decreased，while the apoptosis rate，the level of Bax protein，the relative content of ROS，the concentration of MDA，the levels of TNF-α and IL-1β，and the mRNA and protein levels of TLR4，NF-κB and NLRP3 increased （
P
<
0.05）. Compared with the UVB group，the cell survival rate，the expression levels of PCNA and Bcl-2 proteins，the viabilities of SOD and CAT，and the GSH concentration in the TAK-242 group and CUR group increased，while the apoptosis rate，the level of Bax protein，the relative content of ROS，the concentration of MDA，the levels of TNF-α and IL-1β，and the mRNA and protein levels of TLR4，NF-κB and NLRP3 decreased （
P
<
0.05）. Compared with the CUR group，the cell survival rate，the expression levels of PCNA and Bcl-2 proteins，the viabilities of SOD and CAT，and the GSH concentration in the CUR+LPS group decreased，while the apoptosis rate，the level of Bax protein，the relative content of ROS，the concentration of MDA，the levels of TNF-α and IL-1β，and the mRNA and protein levels of TLR4，NF-κB and NLRP3 increased （
P
<
0.05）.
Conclusion
2
CUR can increase the antioxidant stress level of keratinocytes，alleviate inflammatory response，promote cell proliferation，and improve cell damage caused by UVB irradiation，which may be related to the inhibition of TLR4/NF-κB/NLRP3 signaling pathway.
关键词
Keywords
references
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