The effect of Yang Yan Qing E Wan on senescent phenotypes and the expression of β-catenin and p16INK4a in human skin fibroblasts

Journal of Tissue Viability(2020)

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摘要
This aim of this study was to observe the effect of Yang Yan Qing E Wan (YYQEW) on senescent phenotypes and the expression of β-catenin and p16INK4a in the hydrogen peroxide (H2O2)-induced premature senescence of normal human skin fibroblasts (NHSFs). Primary normal human skin fibroblasts were randomly divided into a normal group, a blank group, a model group, and a YYQEW group. The cells of the model group and the YYQEW group were exposed to 150 μmol/L H2O2 for 2 h. The morphological changes of the cells were analyzed by microscopy and by kits used to estimate the activities of the senescence-associated β-galactosidase (SA-β-gal), reactive oxygen species (ROS), and superoxide dismutase (SOD). The outcomes revealed that dyeing rate proportion of SA-β-gal was 2.78% ± 0.22% in the normal group, 2.83% ± 0.29% in the blank group, 37.58% ± 2.56% in the model group, and 28.39% ± 0.93% in the YYQEW group. The number of SA-β-gal positive cells was thus significantly higher in the model group than in the normal or blank group. There were also fewer SA-β-gal positive cells in the YYQEW group compared with the model group. The expression of ROS and p16INK4a in the model group increased significantly compared with that in the normal or blank groups, while the expression of ROS and p16INK4a in the YYQEW group decreased significantly compared with that in the model group. The expression of SOD and β-catenin in the model group decreased significantly compared with that in the normal or blank group, and the expression of SOD and β-catenin in the YYQEW group increased significantly compared with that in the model group. Overall, it was found that YYQEW was able to delay the senescence of NHSFs induced by H2O2 treatment by alleviating oxidative stress and regulating a number of senescence-related molecules, such as β-catenin and p16INK4a.
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关键词
Yang Yan Qing E Wan,Skin aging,Oxidative stress,β-catenin,p16INK4a
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