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Ginsenoside Rb1, Rg1 and three extracts of traditional Chinese medicine attenuate ultraviolet B‐induced G1 growth arrest in HaCaT cells and dermal fibroblasts involve down‐regulating the expression of p16, p21 and p53
Author(s) -
Wang XiaoYong,
Wang YunGui,
Wang YanFei
Publication year - 2011
Publication title -
photodermatology, photoimmunology and photomedicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.736
H-Index - 60
eISSN - 1600-0781
pISSN - 0905-4383
DOI - 10.1111/j.1600-0781.2011.00601.x
Subject(s) - hacat , cell cycle , cell cycle checkpoint , g1 phase , western blot , cell growth , flow cytometry , chemistry , cell , microbiology and biotechnology , cancer research , traditional medicine , cell culture , biology , medicine , biochemistry , gene , genetics
Objective: The aims of this study were to confirm whether traditional Chinese medicine ginsenoside Rb1 (Rb1), ginsenoside Rg1 (Rg1), polygonum multiflorum (PM), ginkgo extract (GE) and lycium barbarum polysaccharide (LBP) can attenuate G1 growth arrest of HaCaT cells and dermal fibroblasts induced by 10 subcytotoxic ultraviolet B (UVB) exposures, and to explore the possible mechanism in terms of the expression of cell‐cycle regulatory proteins p16, p21 and p53. Methods: Ten subcytotoxic exposures to UVB induced G1 growth arrest of HaCaT cells and dermal fibroblasts. Cell‐cycle analysis was performed using flow cytometry, and mRNA levels of p16, p21 and p53 were detected by a reverse transcription‐polymerase chain reaction (RT‐PCR), and protein levels were detected using Western blot analysis. Results: Five types of traditional Chinese medicine attenuated UVB‐induced G1 growth arrest. The mRNA and protein levels of p16, p21 and p53 in HaCaT cells and dermal fibroblasts increased after UVB irradiation, but pretreatment with five types of traditional Chinese medicine decreased the expression of p16, p21 and p53. Conclusions: These results indicated that five types of traditional Chinese medicine can attenuate G1 growth arrest of HaCaT cells and dermal fibroblasts induced by UVB exposures, which was caused by down‐regulating the expression of cell‐cycle regulatory proteins p16, p21 and p53.