药学学报
藥學學報
약학학보
ACTA PHARMACEUTICA SINICA
2005年
1期
13-16
,共4页
α-青心酮%Na+,K+-ATP酶%线粒体膨胀%脂质过氧化物%耗氧量
α-青心酮%Na+,K+-ATP酶%線粒體膨脹%脂質過氧化物%耗氧量
α-청심동%Na+,K+-ATP매%선립체팽창%지질과양화물%모양량
3,4-dihydroxyacetophenone%Na +,K +-ATPase%mitochondria swelling%lipid peroxidation%oxygen consumption
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.
目的研究α-青心酮對抗壞血痠和硫痠亞鐵誘導腦線粒體Na+,K+-ATPase活性和腦細胞耗氧的作用.方法採用無機燐法測定Na+,K+-ATPase活性,分光光度法檢測腦線粒體膨脹和脂質過氧化物,氧電極法測定腦細胞耗氧量.結果在抗壞血痠和硫痠亞鐵的作用下,鼠腦線粒體Na+,K+-ATPase活性降低,線粒體膨脹和腦細胞脂質過氧化物升高.α-青心酮抑製其抗壞血痠和硫痠亞鐵誘導腦線粒體和細胞的損傷,增加Na+,K+-ATPase活性,降低腦線粒體膨脹和腦細胞脂質過氧化物生成.α-青心酮還具有減少ADP刺激的腦細胞耗氧的作用.結論α-青心酮通過清除自由基和抗氧化作用保護腦細胞結構和功能的完整.
목적연구α-청심동대항배혈산화류산아철유도뇌선립체Na+,K+-ATPase활성화뇌세포모양적작용.방법채용무궤린법측정Na+,K+-ATPase활성,분광광도법검측뇌선립체팽창화지질과양화물,양전겁법측정뇌세포모양량.결과재항배혈산화류산아철적작용하,서뇌선립체Na+,K+-ATPase활성강저,선립체팽창화뇌세포지질과양화물승고.α-청심동억제기항배혈산화류산아철유도뇌선립체화세포적손상,증가Na+,K+-ATPase활성,강저뇌선립체팽창화뇌세포지질과양화물생성.α-청심동환구유감소ADP자격적뇌세포모양적작용.결론α-청심동통과청제자유기화항양화작용보호뇌세포결구화공능적완정.
Aim To investigate the effect of 3,4-dihydroxyacetophenone (α-DHAP) on Na +, K +-ATPase activity of injured brain mitochondria induced by ascorbate-FeSO4 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-FeSO4. 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 FeSO4. 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.