Abstract Objective To examine UVB-induced responses in normal human keratinocytes （HaCaT） and epidermoid carcinoma cells （A431） at the cellular and molecular level, and investigated the protective effect of salidr...Abstract Objective To examine UVB-induced responses in normal human keratinocytes （HaCaT） and epidermoid carcinoma cells （A431） at the cellular and molecular level, and investigated the protective effect of salidroside. Methods Cells irradiated by UVB at various dosage and their viability was assessed by MTT assays, cell cycle was analysed by flow cytometry. The expression of NF-KB, BCL-2, and CDK6 after 50 J/㎡ UVB irradiation were detected by RT-PCR and western blotting. Results Our results confirmed greater tolerance of A341 cells to UVB-induced damage such as cell viability and cell cycle arrest, which was accompanied by differential expression changes in NF-KB, BCL-2, and CDK6. UVB exposure resulted in HaCaT cells undergoing G1-S phase arrest. When treated with salidroside, HaCaT survival was significantly enhanced following exposure to UVB, suggesting great therapeutic potential for this compound. Conclusion Taken together, our study suggests that A431 respond differently to UVB than norma HaCaT cells, and supports a role for NF-KB, CDK6, and BCL-2 in UVB-induced cell G1-S phase arrest Furthermore, salidroside can effectively protect HaCaT from UVB irradiation.展开更多
基金supported by the National Natural Science Foundation of China(30970673,81172634)Natural Science Foundation of Guangdong Province(9151022501000013,S2011040003686)+1 种基金Guangdong Province"211Project"(200826GW,201007GW)Grant from School of Public Health and Tropical Medicine of Southern Medical University,China(Grant No.GW201111)
文摘Abstract Objective To examine UVB-induced responses in normal human keratinocytes （HaCaT） and epidermoid carcinoma cells （A431） at the cellular and molecular level, and investigated the protective effect of salidroside. Methods Cells irradiated by UVB at various dosage and their viability was assessed by MTT assays, cell cycle was analysed by flow cytometry. The expression of NF-KB, BCL-2, and CDK6 after 50 J/㎡ UVB irradiation were detected by RT-PCR and western blotting. Results Our results confirmed greater tolerance of A341 cells to UVB-induced damage such as cell viability and cell cycle arrest, which was accompanied by differential expression changes in NF-KB, BCL-2, and CDK6. UVB exposure resulted in HaCaT cells undergoing G1-S phase arrest. When treated with salidroside, HaCaT survival was significantly enhanced following exposure to UVB, suggesting great therapeutic potential for this compound. Conclusion Taken together, our study suggests that A431 respond differently to UVB than norma HaCaT cells, and supports a role for NF-KB, CDK6, and BCL-2 in UVB-induced cell G1-S phase arrest Furthermore, salidroside can effectively protect HaCaT from UVB irradiation.
