Protective Effects Of Polypeptides From Chlamys Farreri On Murine Thymocytes Damaged By UVB Radiation

AIM We established the irradiation damage models of thymocytes caused by UVB radiation in vitro to study the protective effects and mechanism of PCF (polypeptides from Chlamys farreri) on thymocytes from the mice damaged by UVB radiation (45mJ/cm2). MATHODS The viability of thymocytes were determined by MTT. The intracellular of SOD, GSH-Px, CAT were measured. The production of ROS and the rate of apoptosis on thymocytes were tested using flow cytometry (FCM). The ultrastructure of the cells was observed through electron microscope. Thymocytes were also pretreated with or without ERKs, JNKs and p38 kinase inhibitors prior to UVB irradiation and DNA fragmentation was assessed by agarose gel electrophoresis. The activation of ERKs, JNKs, p38 kinase were investigated by western-blot. RESULTS The results indicated that PCF could significantly increase the viability of thymocytes and enhance the activities of SOD, GSH-Px, CAT in cells. PCF decreased the amounts of ROS and the rate of apoptosis in cells. PCF inhibited the morpholog alteration of the thymocytes irradiated by UVB and maintained the ultrastructure of cells in normal. PCF attenuated UVB caused DNA fragmentation in thymocytes. While combined ERKs inhibitor yielded typical DNA fragmentation, co-treatment of thymocytes with PCF and JNKs and p38 kinase inhibitors completely blocked UVB-induced DNA fragmentation. PCF significantly abolished activation of JNKs and p38 kinase activation while enhanced ERKs activation. CONCLUSION PCF had the protective effects on damages of thymocytes caused by the irradiation of UVB. The mechanisms might be related to increasing anti-oxidative enzymes in thymocytes, inhibiting of the amount of ROS and reducing DNA fragmentation formation. This study suggested that part of the protective function of PCF might be mediated by its ability to modulate the MAPKs signal transduction cascaded.