title: Inhibitory effects of Baicalin on ultraviolet B-induced photo-damage in keratinocyte cell line.
abstract: Baicalin, one kind of Chinese herbal medicine with anti-inflammatory and anti-oxidant property, has been commonly used as a clinical medicine. However, little has been known about the effects of Baicalin on ultraviolet (UV) induced photo-aging and photo-carcinogenesis. The photoproduct is critical to the initial event of UV-induced photo-carcinogenesis. The purpose of the present study was to investigate whether Baicalin, in immortalized human keratinocyte HaCaT cells, could inhibit ultraviolet-B (UVB) induced skin damage and its possible underlying mechanisms, such as inhibiting UVB-induced cytotoxicity and apoptosis, cyclobutane pyrimidine dimers (CPDs), down-regulating the expression of regulatory proteins which are related to cell apoptosis and DNA damage/repair. Our study revealed that Baicalin treatment could inhibit the UVB-induced cytotoxicity, apoptosis and CPD level. It also decreased the mRNA expression of apoptosis-regulatory genes (p53-p21 and c-fos), the protein levels of p53, proliferating cell nuclear antigen (PCNA) and repair protein A (RPA), and the secretion of cytokines [interleukin(IL)-6 and tumor necrosis factor (TNF-alpha)]. These results suggested that Baicalin may have an inhibitory effect on the UVB-induced photo-damage by blocking the relevant cytokine secretion and expression of p53-p21, c-fos, PCNA and RPA genes.
authors: Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, People's Republic of China.
authors: Wei
authors: W
authors: Min
authors: Xiang-Fei
authors: XF
authors: Lin
authors: Xu
authors: X
authors: Miao
authors: Bao-Tao
authors: BT
authors: Wang
authors: Zi-Liang
authors: ZL
authors: Yang
authors: Dan
authors: D
authors: Luo
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects / Q000528:radiation effects; D002460:Cell Line; D050759:Cyclin-Dependent Kinase Inhibitor p21 / Q000378:metabolism; D004249:DNA Damage / Q000187:drug effects / Q000528:radiation effects; D004307:Dose-Response Relationship, Radiation; D004365:Drugs, Chinese Herbal / Q000494:pharmacology*; D005419:Flavonoids / Q000494:pharmacology*; D005786:Gene Expression Regulation / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D015850:Interleukin-6 / Q000378:metabolism; D015603:Keratinocytes / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D016760:Proto-Oncogene Proteins c-fos / Q000378:metabolism; D011740:Pyrimidine Dimers / Q000378:metabolism; D051716:Replication Protein A / Q000378:metabolism; D015595:Skin Aging / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; C493956:CDKN1A protein, human; D050759:Cyclin-Dependent Kinase Inhibitor p21; D004365:Drugs, Chinese Herbal; D005419:Flavonoids; D015850:Interleukin-6; D018809:Proliferating Cell Nuclear Antigen; D016760:Proto-Oncogene Proteins c-fos; D011740:Pyrimidine Dimers; C497167:RPA1 protein, human; D051716:Replication Protein A; D014409:Tumor Necrosis Factor-alpha; D016159:Tumor Suppressor Protein p53; C038044:baicalin