title: Involvement of ROS/ASMase/JNK signalling pathway in inhibiting UVA-induced apoptosis of HaCaT cells by polypeptide from Chlamys farreri.
abstract: Polypeptide from Chlamys farreri (PCF), a novel marine active material isolated from gonochoric Chinese scallop C. farreri, has potential antioxidant activity and protective effect against ultraviolet (UV) irradiation. The aim was to investigate whether PCF protects HaCaT cells from apoptosis induced by UVA and explore related molecular mechanisms. The results showed that PCF significantly prevented UVA-induced apoptosis of HaCaT cells. PCF not only strongly reduced the intracellular reactive oxygen species (ROS) production, but also diminished expression of acid sphingomyelinase (ASMase) and phosphorylated JNK in HaCaT cells radiated by UVA in a dose-dependent manner. Pre-treatment with ROS scavenger NAC, ASMase inhibitor desipramine or JNK inhibitor SP600125 was found to effectively prohibit UVA-induced apoptosis and desipramine markedly blocked phosphorylation of JNK. So it is concluded that PCF obviously protects HaCaT cells from apoptosis induced by UVA and protective effects may attribute to decreasing intracellular ROS level and blocking ASMase/JNK apoptotic signalling pathway.
authors.affiliation: Department of Biochemistry and Molecular Biology, Medical College of Qingdao University, Qingdao, China.
authors.forename: Yan-Xia
authors.initials: YX
authors.lastname: Xing
authors.forename: Ping
authors.initials: P
authors.lastname: Li
authors.forename: Yuan-Xin
authors.initials: YX
authors.lastname: Miao
authors.forename: Wei
authors.initials: W
authors.lastname: Du
authors.forename: Chun-Bo
authors.initials: CB
authors.lastname: Wang
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000818:Animals; D000873:Anthracenes / Q000494:pharmacology; D000975:Antioxidants / Q000302:isolation & purification / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects*; D002460:Cell Line; D003891:Desipramine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004789:Enzyme Activation; D016166:Free Radical Scavengers / Q000494:pharmacology; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015603:Keratinocytes / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D049897:Pectinidae / Q000737:chemistry; D010455:Peptides / Q000302:isolation & purification / Q000494:pharmacology*; D010766:Phosphorylation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects / Q000528:radiation effects; D013108:Sphingomyelin Phosphodiesterase / Q000037:antagonists & inhibitors / Q000378:metabolism*; D014466:Ultraviolet Rays
chemical_list: D000873:Anthracenes; D000975:Antioxidants; D016166:Free Radical Scavengers; D010455:Peptides; D047428:Protein Kinase Inhibitors; D017382:Reactive Oxygen Species; C432165:pyrazolanthrone; D048031:JNK Mitogen-Activated Protein Kinases; D013108:Sphingomyelin Phosphodiesterase; D003891:Desipramine; D000111:Acetylcysteine