title: 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.
abstract: 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.
authors: Department of Dermatology, the First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China. wangxiaoyong1974@163.com
authors: Xiao-Yong
authors: XY
authors: Wang
authors: Yun-Gui
authors: YG
authors: Wang
authors: Yan-Fei
authors: YF
authors: Wang
mesh_terms: D002460:Cell Line; D002491:Central Nervous System Agents / Q000494:pharmacology*; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000096:biosynthesis*; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000096:biosynthesis*; D020405:Dermis / Q000166:cytology / Q000378:metabolism*; D015536:Down-Regulation / Q000187:drug effects / Q000528:radiation effects; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism*; D016193:G1 Phase / Q000187:drug effects / Q000528:radiation effects; D036145:Ginsenosides / Q000494:pharmacology*; D006801:Humans; D008516:Medicine, Chinese Traditional; D016159:Tumor Suppressor Protein p53 / Q000096:biosynthesis*; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: C493956:CDKN1A protein, human; D002491:Central Nervous System Agents; D019941:Cyclin-Dependent Kinase Inhibitor p16; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004365:Drugs, Chinese Herbal; D036145:Ginsenosides; C495901:TP53 protein, human; D016159:Tumor Suppressor Protein p53; C442759:ginsenoside Rb1; C035054:ginsenoside Rg1