title: UV-B induced keratinocyte apoptosis is blocked by 2-selenium-bridged beta-cyclodextrin, a GPX mimic.
abstract: Cell proliferation and cell death of keratinocytes are tightly regulated to ensure epidermal homeostasis. UV-B induces keratinocyte apoptosis. UV-B also induces lipid peroxidation of keratinocytes to increase their amount of malondialdehyde (MDA). These phenomena can be explained by the production of reactive oxygen species (ROS) induced by UV-B radiation. We synthesized 2-selenium-bridged beta-cyclodextrin (2-SeCD) to imitate glutathione peroxidase (GPX), an important antioxidant and established a damage system, in which keratinocytes can be damaged by Ultraviolet B (UV-B) radiation. Using this damage system we studied 2-SeCD protection of keratinocytes against injury induced by UV-B. Experimental results showed that 2-SeCD could protect keratinocytes from apoptosis. Moreover, 2-SeCD inhibits lipid peroxidation of keratinocytes and scavenges ROS. 2-SeCD inhibits the UV-B induced apoptotic signal transduction. This antiapoptotic mechanism may be partly related to the elimination of hydrogen peroxide.
authors.affiliation: Key Laboratory for Molecular Enzymology, Jilin University, 125 Jiefang Road, Changchun 130023, PR China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Mu
authors.forename: Shaowu
authors.initials: S
authors.lastname: Lv
authors.forename: Xiaojun
authors.initials: X
authors.lastname: Ren
authors.forename: Guanghui
authors.initials: G
authors.lastname: Jin
authors.forename: Junqiu
authors.initials: J
authors.lastname: Liu
authors.forename: Ganglin
authors.initials: G
authors.lastname: Yan
authors.forename: Weijia
authors.initials: W
authors.lastname: Li
authors.forename: Jiacong
authors.initials: J
authors.lastname: Shen
authors.forename: Guimin
authors.initials: G
authors.lastname: Luo
mesh_terms: D017209:Apoptosis / Q000187:drug effects* / Q000528:radiation effects*; D001952:Bridged-Ring Compounds / Q000494:pharmacology; D002460:Cell Line; D003505:Cyclodextrins / Q000494:pharmacology*; D016166:Free Radical Scavengers / Q000494:pharmacology; D005979:Glutathione Peroxidase / Q000378:metabolism; D006801:Humans; D015603:Keratinocytes / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism / Q000528:radiation effects*; D015227:Lipid Peroxidation / Q000187:drug effects; D018716:Molecular Mimicry; D016566:Organoselenium Compounds / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects; D014466:Ultraviolet Rays / Q000009:adverse effects*; D047392:beta-Cyclodextrins
chemical_list: C426831:6A,6B-diseleninic acid-6A',6B'-selenium bridged beta-cyclodextrin; D001952:Bridged-Ring Compounds; D003505:Cyclodextrins; D016166:Free Radical Scavengers; D016566:Organoselenium Compounds; D017382:Reactive Oxygen Species; D047392:beta-Cyclodextrins; D005979:Glutathione Peroxidase