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目的:建立中波紫外线(UVB)对体外培养的永生化人角质形成细胞(HaCaT细胞)辐射损伤病理模型,探讨姜黄素(Cur)对其细胞辐射损伤的保护作用。方法:以10、20、30、40和50m J/cm2的UVB辐照其细胞,分别在辐照后6、12、18、24、48和72h,用MTT和流式细胞仪检测细胞活性及其凋亡的变化,建立辐照损伤病理模型;用30m J/cm2的剂量辐照其细胞后,立即分别给予0.625、1.25、2.5和5μg/mL的Cur处理,在处理18h后检测其细胞凋亡。结果:HaCaT细胞经UVB辐照后,以剂量和时间依赖方式抑制其细胞存活,且主要由于细胞凋亡引起;Cur以浓度依赖方式抑制由UVB所致的细胞凋亡。结论:Cur能抑制UVB辐射诱导的HaCaT细胞凋亡,对UVB辐射损伤HaCaT细胞具有保护作用,其作用机制可能与Cur清除体内自由基而增强细胞的抗氧化能力有关。
OBJECTIVE: To establish a pathological model of radiation damage of immortalized human keratinocytes (HaCaT cells) cultured in vitro by ultraviolet (UVB), and to investigate the protective effects of curcumin (Cur) on radiation damage to cells. METHODS: The cells were irradiated with UVB at 10, 20, 30, 40, and 50 m J/cm2. The cell viability was measured by MTT and flow cytometry at 6, 12, 18, 24, 48, and 72 hours after irradiation. Apoptosis changes were established to establish a pathological model of radiation injury; after irradiated with a dose of 30 mJ/cm2, the cells were immediately treated with Cur at 0.625, 1.25, 2.5, and 5 μg/mL, and their cell death was measured at 18 h after treatment. Died. RESULTS: After UVB irradiation, HaCaT cells inhibited cell survival in a dose- and time-dependent manner and were mainly caused by apoptosis. Cur inhibited UVB-induced apoptosis in a concentration-dependent manner. CONCLUSION: Cur inhibits the apoptosis of HaCaT cells induced by UVB radiation and protects HaCaT cells against UVB radiation. The mechanism may be related to the fact that Cur scavenges free radicals and enhances the antioxidant capacity of cells.