盐藻β-胡萝卜素对^(60)Co辐射引起小鼠胸腺淋巴细胞凋亡的影响

Effects of β-carotene from Dunaliella on thymocytes apoptosis caused by ^(60)Co irradiation in mice

目的探讨盐藻β-胡萝卜素(p-C)对^(60)Co辐射引起小鼠胸腺淋巴细胞凋亡的影响。方法建立^(60)Co辐射(强度为3Gy)体外培养的小鼠胸腺淋巴细胞损伤病理模型。透射电镜观察盐藻β-C对^(60)Co辐射引起小鼠胸腺淋巴细胞超微结构变化;MTT法测定小鼠胸腺淋巴细胞的活性;Brdu法测定盐藻β-C对小鼠胸腺淋巴细胞增殖状态的影响;琼脂糖凝胶电泳观察细胞凋亡情况;Western blot测定p38及磷酸化p38蛋白的表达。结果盐藻β-C能减轻^(60)Co辐射所致的胸腺淋巴细胞凋亡的形态学改变;能显著提高细胞活性,使处于增殖状态的细胞显著增多;能减少^(60)Co辐射所致淋巴细胞DNA梯状带的出现,降低淋巴细胞凋亡率;能抑制^(60)Co辐射后小鼠胸腺淋巴细胞P38蛋白的磷酸化。结论盐藻β-C能抑制^(60)Co辐射诱导的淋巴细胞凋亡,对^(60)Co辐射损伤的小鼠胸腺淋巴细胞具有保护作用。其作用机制可能与盐藻β-C乳剂能清除氧自由基、减少DNA的断裂、抑制磷酸化p38蛋白的表达有关。

Objective To study the effects of β-carotene from Dunallia （β-C） on apoptosis induced by ^60Co γ-ray in routine thymocytes. Methods The irradiation damage models of thymocytes by ^60Co γ-ray（3Gy） were established. The ultrastructure of the cells were observed by electron microscope. The viability of thymocytes were determined by MTT. Cell proliferation were investigated by Brdu method. The apoptosis was assessed by agarose gel electrophoresis. The activation of p38 kinase was investigated by Western-blot. Results β-C inhibited the morphologic alteration of the thymocytes irradiated by ^60Co γ-ray and maintained the ultrastructure of ceils in normal. β-C increased the viability of thymocytes and enhanced the abilities of cell proliferation. β-C attenuated ^60Co γ-ray caused DNA fragmentation in thymocytes, and abolished activation of p38 kinase. Conclusion β-C has protective effects on damages of thymocytes caused by ^60Co irradiation, whose mechanism might be related to scavenge oxyradical,decrease DNA fragmentation, and inhibit the expression of phosphorylated p38.