二苯乙烯苷可抑制中波紫外线诱导的人皮肤成纤维细胞光老化

目的: 研究二苯乙烯苷（TSG）对紫外线B（UVB）诱导的人皮肤成纤维细胞（HSF）应激性提早衰老的作用及可能的机制。方法: UVB小剂量、多次照射HSF，每次照射完毕后分别用0.02、0.10、0.50 mmol/L浓度的TSG处理。实验分为6组：空白对照组、模型对照组、UVB+0.02 mmol/L TSG组、UVB+0.10 mmol/L TSG组、UVB+0.50 mmol/L TSG组、TSG对照组。采用细胞计数法（CCK-8）检测细胞增殖活性；细胞化学染色法检测衰老相关β-半乳糖苷酶（SA-β-gal）表达；TBA法、WST-1法测定细胞丙二醛（MDA）含量和超氧化物歧化酶（SOD）活性；ELISA法测定细胞上清液中基质金属蛋白酶-1（MMP-1）的含量变化。结果: 与空白对照组比较，模型对照组细胞增殖活性减弱（P < 0.05），SA-β-gal染色呈强阳性，细胞裂解液中SOD活性减弱、MDA含量增加，MMP-1浓度升高（P < 0.05或P < 0.01）。与模型对照组比较，UVB+各浓度TSG组细胞增殖活性改善（均P < 0.05），SA-β-gal染色阳性率下降，细胞裂解液中SOD活性增强、MDA含量减少，MMP-1浓度减小（P < 0.05或P < 0.01）。结论: TSG可以在一定程度上抑制UVB诱导的HSF应激性提早衰老，该作用可能与改善氧化应激、抑制MMP-1高表达有关。

Stilbene glucoside inhibits ultraviolet radiation B-induced photoaging in human skin fibroblasts

Objective: To study the effects of tetrahydroxy stilbene-2-O-β-D-glucoside (TSG) on stress-induced premature senescence of human skin fibroblasts (HSF) exposed to ultraviolet radiation B (UVB) and its possible mechanism. Methods: HSFs were repeatedly exposed to UVB at a subcytotoxic level. TSG treatment (0.02, 0.10 and 0.50 mmol/L) was given immediately after each irradiation. The HSFs were divided into six groups:blank control group, model group, UVB+0.02 mmol/L TSG group, UVB+0.10 mmol/L TSG group, UVB+0.50 mmol/L TSG and TSG group (0.50 mmol/L). Cell counting kit-8 (CCK-8) was used to evaluate the proliferative activity of cells; senescence-associated-β-galactosidase (SA-β-gal) staining was performed to estimate the degree of premature senescence in cells; TBA method and WST-1 method were used to detect intracellular malondialdehyde (MDA) and superoxide dismutase (SOD) activities; and ELISA was applied to quantify the secretion level of matrix metalloproteinase1 (MMP-1) in cultured supernatant. Results: Compared with the blank control group, the proliferative activity and SOD level in the model group decreased (P < 0.05), while the percentage of SA-β-gal-positive cells, MDA and MMP-1 levels increased (P < 0.05 or P < 0.01). Compared with the model group, the proliferative activity and SOD level increased in UVB+TSG groups (all P < 0.05), and the percentage of SA-β-gal-positive cells, MDA and MMP-1 levels decreased (P < 0.05 or P < 0.01). Conclusion: TSG can inhibit UVB-induced premature senescence of HSF, which may be related to the inhibition of oxidative stress and high expression of MMP-1.