title: Effects of baicalin against UVA-induced photoaging in skin fibroblasts.
abstract: Ultraviolet A (UVA) radiation contributes to skin photoaging. Baicalin, a plant-derived flavonoid, effectively absorbs UV rays and has been shown to have anti-oxidant and anti-inflammatory properties that may delay the photoaging process. In the current study, cultured human skin fibroblasts were incubated with 50 μg/ml baicalin 24 hours prior to 10 J/cm(2) UVA irradiation. In order to examine the efficacy of baicalin treatment in delaying UVA-induced photoaging, we investigated aging-related markers, cell cycle changes, anti-oxidant activity, telomere length, and DNA damage markers. UVA radiation caused an increased proportion of β-Gal positive cells and reduced telomere length in human skin fibroblasts. In addition, UVA radiation inhibited TGF-β1 secretion, induced G1 phase arrest, reduced SOD and GSH-Px levels, increased MDA levels, enhanced the expression of MMP-1, TIMP-1, p66, p53, and p16 mRNA, reduced c-myc mRNA expression, elevated p53 and p16 protein expression, and reduced c-myc protein expression. Baicalin treatment effectively protected human fibroblasts from these UVA radiation-induced aging responses, suggesting that the underlying mechanism involves the inhibition of oxidative damage and regulation of the expression of senescence-related genes, including those encoding for p53, p66(Shc) and p16.
authors.affiliation: Department of Dermatology, The First Affiliated Hospital of Soochow University, Suzhou, China , Department of Dermatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
authors.forename: Wei
authors.initials: W
authors.lastname: Min
authors.forename: Xin
authors.initials: X
authors.lastname: Liu
authors.forename: Qihong
authors.initials: Q
authors.lastname: Qian
authors.forename: Bingjiang
authors.initials: B
authors.lastname: Lin
authors.forename: Di
authors.initials: D
authors.lastname: Wu
authors.forename: Miaomiao
authors.initials: M
authors.lastname: Wang
authors.forename: Israr
authors.initials: I
authors.lastname: Ahmad
authors.forename: Nabiha
authors.initials: N
authors.lastname: Yusuf
authors.forename: Dan
authors.initials: D
authors.lastname: Luo
mesh_terms: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D002453:Cell Cycle / Q000187:drug effects; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000235:genetics* / Q000528:radiation effects*; D019941:Cyclin-Dependent Kinase Inhibitor p16; D004249:DNA Damage / Q000187:drug effects; D005347:Fibroblasts / Q000166:cytology / Q000378:metabolism / Q000528:radiation effects*; D005419:Flavonoids / Q000494:pharmacology*; D015870:Gene Expression / Q000187:drug effects / Q000528:radiation effects; D006801:Humans; D009363:Neoplasm Proteins / Q000378:metabolism; D055765:Shc Signaling Adaptor Proteins / Q000378:metabolism; D012867:Skin / Q000166:cytology* / Q000528:radiation effects*; D015595:Skin Aging / Q000235:genetics* / Q000528:radiation effects*; D000071425:Src Homology 2 Domain-Containing, Transforming Protein 1; D059505:Telomere Homeostasis / Q000187:drug effects; D053773:Transforming Growth Factor beta1 / Q000378:metabolism; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; C000614131:CDKN2A protein, human; D019941:Cyclin-Dependent Kinase Inhibitor p16; D005419:Flavonoids; D009363:Neoplasm Proteins; C528024:SHC1 protein, human; D055765:Shc Signaling Adaptor Proteins; D000071425:Src Homology 2 Domain-Containing, Transforming Protein 1; D053773:Transforming Growth Factor beta1; D016159:Tumor Suppressor Protein p53; C038044:baicalin