Meijiao Xu1,2, Yifeng Wang2,3. 1. Department of Dermatology, Suzhou Dushuhu Public Hospital, Dushuhu Public Hospital Affiliated to Soochow University, Suzhou 215000, China. 2. The Second Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou 310053, China. 3. Department of Dermatology, Tongde Hospital of Zhejiang Province, Hangzhou 310012, China.
Abstract
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). CONCLUSIONS: 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.
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). CONCLUSIONS: 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.