摘要
目的 研究α- 青心酮对抗坏血酸和硫酸亚铁诱导脑线粒体Na+,K+ ATPase活性和脑细胞耗氧的作用。方法 采用无机磷法测定Na+,K+ ATPase活性,分光光度法检测脑线粒体膨胀和脂质过氧化物,氧电极法测定脑细胞耗氧量。结果 在抗坏血酸和硫酸亚铁的作用下,鼠脑线粒体Na+,K+ ATPase活性降低,线粒体膨胀和脑细胞脂质过氧化物升高。α- 青心酮抑制其抗坏血酸和硫酸亚铁诱导脑线粒体和细胞的损伤,增加Na+,K+ ATPase活性,降低脑线粒体膨胀和脑细胞脂质过氧化物生成。α- 青心酮还具有减少ADP刺激的脑细胞耗氧的作用。结论 α- 青心酮通过清除自由基和抗氧化作用保护脑细胞结构和功能的完整。
Aim To investigate the effect of 3,4-dihydroxyacetophenone (α-DHAP) on Na+,K+-ATPase activity of injured brain mitochondria induced by ascorbate-FeSO_4 and the oxygen consumption of rat brain cells stimulated by ADP. Methods Na+,K+-ATPase activity was determined according to the method of inorganic phosphate. Swelling of the brain mitochondria was detected with the method of spectrophotometer. Lipid peroxidation was detected according to the thiobarbituric acid method of spectrophotometer. Oxygen consumption was measured by oxygen electrode method. Results The decrease of Na+,K+-ATPase activity, mitochondria swelling and formation of lipid peroxidation were shown in rat brain mitochondria and cells induced by ascorbate-FeSO_4. α-DHAP was shown to increase the activity of Na+,K+-ATPase, decrease the mitochondria swelling and inhibit the production of lipid peroxidation of brain mitochondria and cells induced by ascorbate and FeSO_4. α-DHAP can also reduce the oxygen consumption of brain cells stimulated by ADP. Conclusion α-DHAP can protect the structure and the function of brain mitochondria and cells by scavenging the free radical and resisting the reaction of lipid peroxidation.
出处
《药学学报》
CAS
CSCD
北大核心
2005年第1期13-16,共4页
Acta Pharmaceutica Sinica