甘草次酸对光老化HaCaT细胞的保护作用及NF-κB信号通路影响

The Protective Role of Glycyrrhizin on Light Aging of HaCaT Cell and the NF-κB Signaling Pathway

目的:研究甘草次酸对光老化人皮肤角质形成细胞(HaCaT)的保护作用及NF-κB信号通路的影响。方法:用30m J/cm2的UVB照射HaCaT细胞,建立光老化模型;用不同浓度(10^(-7)、10^(-6)、10^(-5)mol·L^(-1))的甘草次酸处理光老化HaCaT细胞24h。MTT法检测甘草次酸对细胞活性的影响;试剂盒法检测各组细胞上清SOD、GSH活性及MDA含量;Western Blot法检测各组细胞NF-κBP50和NF-κBP65蛋白表达量。结果:模型组细胞与空白组细胞相比,模型组细胞增殖率显著降低(P<0.01);GSH、SOD活性显著降低,MDA含量显著升高(P<0.01);NF-κBP50、NF-κBP65蛋白表达量显著升高(P<0.01)。甘草次酸处理的HaCaT细胞与模型组细胞相比,甘草次酸组细胞增殖率显著升高(P<0.01);GSH、SOD活性显著升高,MDA含量显著降低(P<0.01);NF-κBP50、NF-κBP65蛋白表达显著下降(P<0.05,P<0.01)。结论:甘草次酸能显著保护UVB诱导的HaCaT细胞光老化,其机制可能与其抑制氧化损伤,阻断NF-κB信号通路,抑制NF-κBP50、NF-κBP65蛋白表达有关。

Objective To study the protective role of glycyrrhizin on light aging of HaCaT cell and the NF-κB signaling pathway. Methods Light aging model was set up by the irradiation of ultraviolet radiation B （UVB） at irradiation dose of 30mJ/cm2, （10-7,10-6,10-5） mol·L-1 glycyrrhizin were used to treat the light aging model.The activity of cells was determined by MTT method. The test kits were tested to determine the levels of SOD, GSH activity and the content of MDA in each group of cells.Western blot method was used for the detection of effects of estradiol and isopsoralen on NF-κ BP50 and NF- κBP65 protein expression. Results Compared with the blank group, the cell proliferation rate of the model group significantly decreased（P〈0.01）, the activity of SOD and GSH was significantly decreased, the content of MDA was significantly increased（P〈0.01）, the expression of NF-κBP50 and NF-κBP65 was increased （P〈0.05 or P〈0.01）. Compared with the model group, the cell proliferation rate of the （10-7,10-6,1015） moloL-lglycyrrhizin group significantly increased （P〈0.01）. The activity of SOD and GSH was increased（P〈0.01）. The content of MDA was significantly decreased（P〈0.01）. The expression of NF-κBP50 and NF-κ BP65 was decreased （P〈0.05 or P〈0.01）. Conclusion The glycyrrhizin can significantly protect HaCaT cells light aging, the mechanism may be related with suppress the oxidative damage, blockting NF-κBsignaling pathways, and inhibiting the expression of NF-κBP50 and NF-κBP65.