Calcium mechanism in neurotoxicity induced by soluble A?_ (25-35) on pheochromocytoma cell lines
- VernacularTitle:?-淀粉样蛋白_(25-35)片段致大鼠嗜铬细胞瘤细胞损伤的钙离子机制
- Author:
Mei SHAO
;
Shengdi CHEN
;
Zhenguo LIU
- Publication Type:Journal Article
- Keywords:
Amyloid beta-protein;
Calcium;
PC12 cells;
Alzheimer′s disease
- From:
Chinese Journal of Neurology
2000;0(04):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the calcium mechanism involved in the A? 25-35-induced neurotoxicity.Methods PC12 cells viability was detected by using MTT assay. Relative change of intracellular calcium concentration was measured by laser confocal microscope.Results MTT assay showed that the cell viability of the three groups (10 ?mol/L A? 25-35?10 ?mol/L A? 25-35+5 ?mol/L nifedipine?10 ?mol/L A? 25-35+10 ?mol/L nifedipine) was decreased by 34.5%, 25.1% and 11.0%,as compared with the control group. 10 ?mol/L nifedipine could protect PC12 cells from A? 25-35-induced damage. A? 25-35 of different concentration (0.1 ?mol/L, 1 ?mol/L, 10 ?mol/L, 20 ?mol/L and 30 ?mol/L) resulted in the elevation of intracellular calcium (about 6.38%, 6.42%, 62.2%, 69.3% and 107.5%) with a dose-dependent manner. Potassium (5 mmol/L, 15 mmol/L and 30 mmol/L) could increase the intracellular calcium after one minute pretreatment of different concentration A? 25-35. Both above mentioned actions were sensitive to the medium calcium and were antagonized by nifedipine, a L-voltage-gated calcium channel antagonist.Conclusion Soluble A? 25-35 may damage the neuronal calcium homeostasis in early stage and make neurons more vulnerable to physiological or pathological stimuli.
