9-(4-Ethoxycarbonylphenoxy)-6,7-dimethoxy-1,2,3,4-tetrahydro acridine inhibits free radical induced rat cortical neuron cytotoxicity and cerebral ischemia injury
- VernacularTitle:9-(4-乙氧羰基苯氧基)-6,7-二甲氧基-1,2,3,4-四氢吖啶盐酸盐抑制自由基诱发鼠皮层神经元毒性及脑缺血损伤
- Author:
Rui SHENG
;
Guoqing LIU
- Publication Type:Journal Article
- Keywords:
9-(4-ethoxycarbonylphenoxy)-6,7-dimethoxy-1,2,3,4-tetrahydro acridine;
free radical;
cell culture;
neuron;
cerebral ischemia;
learning and memory
- From:
Acta Pharmaceutica Sinica
2003;38(5):337-341
- CountryChina
- Language:Chinese
-
Abstract:
Aim To study the effects of 9-(4-ethoxycarbonylphenoxy)-6,7-dimethoxy-1,2,3,4-tetrahydro acridine (EDT) on free radical induced injury in primary cultured rat cortical neuron and cerebral ischemia in mice. Methods In primary rat cortical neuron, free radical injury model was established by 10 μmol*L-1 H2O2. The content of malondiadehyde (MDA) and activity of superoxide dismutase (SOD) in cells were investigated. Chronic cerebral ischemia model was produced by occlusion of one carotid artery and pneumogastric nerve in mice. The step down test was adopted to investigate the effect of EDT on the memory impairment. The cerebra morphology and MDA, NO content and SOD activity in mice cerebra were detected. Results In primary rat cortical culture, 0.01-3 μmol*L-1 EDT concentration-dependently inhibited the formation of MDA and reduction of SOD activity induced by 10 μmol*L-1 H2O2. In chronic cerebral ischemia, EDT 2.5, 5 and 10 mg*kg-1 ig for 5 d greatly improved the memory impairment, reduced NO efflux and MDA content, while increased SOD activity in mice cerebra. Conclusion EDT was found to protect neurons from H2O2-induced neurotoxicity and inhibit chronic cerebral ischemia mediated injury and memory impairment in mice.
