Open AccessMolecular mechanisms of polypeptide from Chlamys farreri protecting HaCaT cells from apoptosis induced by UVA plus UVB 1
Author(s) -
GAO Mingqing,
GUO Shenbo,
CHEN Xuehong,
DU Wei,
WANG Chunbo
Publication year - 2007
Publication title -
acta pharmacologica sinica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.514
H-Index - 90
eISSN - 1745-7254
pISSN - 1671-4083
DOI - 10.1111/j.1745-7254.2007.00594.x
Subject(s) - hacat , apoptosis , reactive oxygen species , agarose gel electrophoresis , microbiology and biotechnology , superoxide dismutase , kinase , chemistry , biochemistry , intracellular , biology , oxidative stress , in vitro , dna
Aim : To investigate the mechanism of polypeptide from Chlamys farreri (PCF) protecting HaCaT cells from apoptosis induced by UVA plus UVB in vitro . Methods : An apoptotic model of UV irradiation‐induced HaCaT cells was established. The 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide assay, agarose gel electrophoresis, biochemical methods, and Western blotting were employed in the study. Results : PCF inhibited the UV irradiation‐induced apoptosis of HaCaT cells. PCF strongly reduced the intracellular reactive oxygen species level, enhanced activities of superoxide dismutase and glutathione peroxidase and increased the total anti‐oxidative capacity in HaCaT cells following UV irradiation. Furthermore, we found that PCF could inhibit the phosphorylation of c‐Jun amino‐terminal kinase and the activity of caspase‐3 in a concentration‐dependent manner. Conclusion : PCF protected HaCaT cells from apoptosis induced by UVA plus UVB, mainly through decreasing the intracellular ROS level and increasing the activities of anti‐oxidative enzymes to block the ROS‐JNKcaspase‐3‐apoptosis signaling pathway.