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目的:观察放线菌素D(ActD)和肿瘤坏死因子α(TNF-α)对大鼠肾上腺嗜铬细胞(PC12细胞)的协同损伤作用,探讨中药单体姜黄素对这种损伤的保护作用及机制。方法:采用MTT法确定实验药物的最佳浓度;LDH法检测PC12细胞的损伤;倒置显微镜观察细胞形态变化;caspase-3活性检测试剂盒检测caspase-3的活性。结果:ActD/TNF-α可致PC12细胞的生存力下降(P<0.05);细胞培养液中LDH的活性升高(P<0.05);PC12数量减少,体积缩小,突起变短;可致PC12细胞内caspase-3的活化增强(P<0.05)。浓度为5μmol/L姜黄素可阻止ActD/TNF-α所致的细胞的生存力下降(P<0.05);抑制ActD/TNF-α引起的细胞培养液中LDH的活性升高(P<0.05);拮抗ActD/TNF-α引起的细胞数量减少,体积变小,突起减少变短;抑制ActD/TNF-α引起的PC12细胞内caspase-3的活化(P<0.05)。结论:姜黄素可以拮抗ActD/TNF-α协同作用引起的PC12细胞损伤,其机制可能与抑制caspase-3的活化有关。
Objective: To observe the synergistic effect of actinomycin D (ActD) and tumor necrosis factor α (TNF-α) on rat adrenal chromaffin cells (PC12 cells), and to explore the protective effect of Chinese traditional medicine curcumin on this injury And mechanism. Methods: MTT method was used to determine the optimal concentration of experimental drugs. The injury of PC12 cells was detected by LDH method. The morphological changes of cells were observed by inverted microscope. The activity of caspase-3 was detected by caspase-3 activity assay kit. Results: The viability of PC12 cells was decreased by ActD / TNF-α (P <0.05), the activity of LDH in cell culture medium was increased (P <0.05), the number of PC12 was decreased, the volume was reduced, Activation of intracellular caspase-3 increased (P <0.05). Curcumin at a concentration of 5 μmol / L prevented the viability of ActD / TNF-α-induced cells from decreasing (P <0.05), and inhibited the increase of LDH activity in ActD / TNF- ; ActD / TNF-αinhibited the number of cells decreased, the volume became smaller and the number of protuberance decreased and the activation of caspase-3 in PC12 cells induced by ActD / TNF-αwas inhibited (P <0.05). Conclusion: Curcumin can antagonize the synergistic effect of ActD / TNF-α on PC12 cell injury, which may be related to the inhibition of caspase-3 activation.