中文摘要：

目的：探讨姜黄素对放线菌素D（ActD）/TNF-α诱导的PC12细胞和大鼠海马神经元凋亡的影响及其作用机制.方法：将PC12细胞分为以下6组：对照组、TNF-α组、ActD组、姜黄素组、ActD/TNF-α组和姜黄素＋ActD/TNF-α组.各组细胞培养24 h后进行下列处理：倒置荧光显微镜普通光观察各组细胞的形态变化;Annexin V/PI染色流式细胞术检测各组PC12细胞凋亡率; Fluo-3 AM染色流式细胞术测定细胞内Ca2＋浓度.制备离体大鼠海马脑片,分组处理同PC12细胞,细胞外微电极记录技术观察各组海马脑片CA1区长时程增强（long-term potentiation,LTP）的变化情况.结果：10 μg/L ActD和50 μg/L TNF-α协同处理可导致PC12细胞明显损伤,而5 μmol/L姜黄素则可以减轻这种损伤作用（P〈0.05）;ActD/TNF-α可诱导PC12细胞内Ca2＋浓度升高,姜黄素可以通过降低胞内Ca2＋浓度而减少ActD/TNF-α引起的细胞凋亡（P〈0.05）.此外,LTP实验也证实ActD/TNF-α可以显著抑制大鼠海马脑片LTP的诱发,而姜黄素可以拮抗这种抑制作用,改善神经元突触可塑性（P〈0.05）.结论：姜黄素可以改善ActD/TNF-α引起的神经元损伤,其机制可能是通过降低细胞内Ca2＋浓度,维持胞内钙稳态而发挥作用.

英文摘要：

AIM： To study the possible mechanism of cureumin on actinomycin D （ActD）/tumor necrosis factor ot （TNF-α） -induced injury in PC12 cells and rat hippocampal neurons. METHODS： PC12 cells wore divided into control group, TNF α group, ActD group, curcumin group, ActD/TNF - α group and curcumin ＋ ActD/TNF - α group. The cells were cultured for 24 h. Inverted fluorescence microscopy was used to observe the morphological changes of the ceils in each group. Annexin V/PI double staining was applied to analyze the apoptosis of PC12 ceils. The level of intracellular Ca2＋ was detected by Fluo -3 AM staining. Rat hippocampal slices were prepared and divided into the same groups as the PC12 cells. Extracellular microelectrode recording technique was used to observe and calculate the changes of long - term potentiation （LTP） in different groups. RESULTS： Apoptosis of PC12 ceils was induced by ActD/TNF-α. Curcumin protected the PCI2 cells from ActD/TNF- α- induced apoptosis （P 〈 0. 05）. ActD/TNF-α increased the intracellular Ca2＋ concentration. Curcumin significantly reduced ActD/TNF - α - induced apoptosis by decreasing the intraeellular Ca2＋ concentration （P 〈 0. 05 ）, inversed the effect of ActD/TNF -α on LTP in hippocampal slices, and improved the synaptic plasticity （ P 〈 0. 05 ）. CONCLUSION： Curcumin protects ActD/TNF - α - induced neuronal damage by depressing the intracellular Ca2＋ concentration and maintaining the homostasis of intracellular calcium.