摘要
目的研究氯胺酮对谷氨酸 (Glu)所致神经性PC12细胞株损伤的保护作用。方法PC12细胞株 (2× 10 3 /mL)在含10nmol/L 7S NGF的培养基中孵育 6d后 ,分化为神经性PC12细胞株。分别加入Glu、氯胺酮、Glu +氯胺酮、D AP5 +Glu +氯胺酮、CNQX +Glu并共同孵育 18h ,以MTT法测细胞活力。结果 30mmol/LGlu与神经性PC12细胞株共同孵育 18h ,细胞活力降至5 %以下。氯胺酮与Glu同时加入 ,对细胞活力有明显保护作用 ,且呈剂量依赖性。 0 .1mmol/L氯胺酮使细胞活力升至 (30 .94±11.75 ) % ;1.0mmol/L氯胺酮组细胞活力为 (95 .74± 2 1.4 9) % ;非NMDA受体拮抗剂 2 0 μmol/LCNQX细胞活力为 (19.31± 5 .83) % ,与Glu对照组比较均有显著差异 (P <0 .0 5或P <0 .0 1)。结论氯胺酮对Glu损伤的神经性PC12细胞具有保护作用 。
Objective Effects of ketamine on glutamate-induced neuronal injury based on PC12 pheochromocytoma cells were studied. Methods PC12 cells were seeded in 96-well plates (2×10 3/mL) in culture medium supplemented with 10 nmol/L mouse 7S-NGF before assay to allow neural differentiation. After 6 d with NGF, glutamate, ketamine, ketamine plus glutamate, D-AP5 plus glutamate plus ketamine, or CNQX plus glutamate were added directly to the cultured cells to achive the desired concentration, and incubated for 18 h before viability was determined by the ability to reduce the tetrazolium derivative, MTT into a blue formazan salt. Results Following the incubation with glutamate (30 mmol/L) for 18 h, the viability of the culture was reduced to <5%. However, ketamine, when added to the incubation medium together with glutamate, inhibited glutamate-induced death in a dose-dependent fashion. Glutamate-induced death was inhibited by (30.94±11.75)% using 0.1 mmol/L ketamine,by (95.74±21.49)% using 1.0 mmol/L ketamine and by (19.31±5.83)% using 20 μmol/L CNQX (P<0.05 or P<0.01). Conclusion Non-competitive antagonist ketamine abrogated the cell death. These data suggest that ketamine promotes PC12 cell survival through glutamate receptor suppression.
出处
《上海第二医科大学学报》
CSCD
2004年第11期894-896,900,共4页
Acta Universitatis Medicinalis Secondae Shanghai
