title: Paeoniflorin attenuates ultraviolet B-induced apoptosis in human keratinocytes by inhibiting the ROS-p38-p53 pathway.
abstract: Ultraviolet (UV) light is one of the most harmful environmental factors that contribute to skin damage. Exposure to UV induces extensive generation of reactive oxygen species (ROS), and results in photoaging and skin cancer development. One approach to protecting human skin against UV radiation is the use of antioxidants. In recent years, naturally occurring herbal compounds have gained considerable attention as protective agents for UV exposure. Paeoniflorin (PF) is a novel natural antioxidant, which is isolated from peony root (Radix Paeoniae Alba). The present study evaluated the protective effects of PF on UV‑induced skin damage in vitro, and demonstrated that the effects were mediated via the ROS‑p38‑p53 pathway. The results of the present study demonstrated that treatment with PF (25, 50, and 100 µM) significantly increased the percentage of viable keratinocytes after UV‑B exposure. In addition, cell death analysis indicated that PF treatment markedly reduced UV‑B‑radiation‑induced apoptosis in keratinocytes, which was accompanied by increased procaspase 3 expression and decreased cleaved caspase 3 expression. Treatment with PF markedly reduced the production of ROS, and inhibited the activation of p38 and p53 in human keratinocytes, thus suggesting that the ROS‑p38‑p53 pathway has a role in UV‑B‑induced skin damage. In conclusion, the present study reported that PF was able to attenuate UV‑B‑induced cell damage in human keratinocytes. Notably, these effects were shown to be mediated, at least in part, via inhibition of the ROS-p38-p53 pathway.
authors.affiliation: Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
authors.forename: Lingwen
authors.initials: L
authors.lastname: Kong
authors.affiliation: Department of Dermatology, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
authors.forename: Shangshang
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Integrative Medicine, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
authors.forename: Xiao
authors.initials: X
authors.lastname: Wu
authors.affiliation: Department of Dermatology, East Hospital, Tongji University School of Medicine, Shanghai 200120, P.R. China.
authors.forename: Fuguo
authors.initials: F
authors.lastname: Zuo
authors.affiliation: Department of Dermatology, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
authors.forename: Haihong
authors.initials: H
authors.lastname: Qin
authors.affiliation: Department of Dermatology, Huashan Hospital, Fudan University, Shanghai 200040, P.R. China.
authors.forename: Jinfeng
authors.initials: J
authors.lastname: Wu
mesh_terms: D000975:Antioxidants / Q000737:chemistry / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects* / Q000528:radiation effects; D015153:Blotting, Western; D053148:Caspase 3 / Q000378:metabolism; D002460:Cell Line; D005960:Glucosides / Q000737:chemistry / Q000494:pharmacology*; D006801:Humans; D015603:Keratinocytes / Q000166:cytology / Q000378:metabolism; D039821:Monoterpenes / Q000737:chemistry / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism; D014466:Ultraviolet Rays; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism; D006027:Glycosides
chemical_list: D000975:Antioxidants; D053148:Caspase 3; D005960:Glucosides; D039821:Monoterpenes; D017382:Reactive Oxygen Species; D016159:Tumor Suppressor Protein p53; D048051:p38 Mitogen-Activated Protein Kinases; C015423:peoniflorin; D006027:Glycosides