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作 者:高湘[1] 张振明[1] 许爱霞[1] 杨社华[1] 王彩琴[1] 李文俊[1]
出 处:《中国医院药学杂志》2006年第9期1051-1053,共3页Chinese Journal of Hospital Pharmacy
基 金:甘肃省中医药科研课题项目(2003-GZK-51)
摘 要:目的:观察中药祛癍方水提物对衰老小鼠模型丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-PX)和脑组织中脂褐质(LF)的影响。方法:用D-半乳糖(D-gal)造衰老小鼠模型,同时灌胃给予方剂药材3.3,6.5,13,26g.kg-1.d-1的水提物,qd,共7周,分别用TBA比色法、亚硝酸盐法、DTNB法及Sohal法测定心、肝、肾组织中MDA,SOD,GSH-PX和脑组织中LF。结果:灌胃给予方剂药材3.3,6.5,13,26g.kg-1.d-1的水提物,能不同程度对抗衰老模型小鼠脑组织中LF升高及心、肝、肾组织中MDA升高,其量效关系均呈负相关,r分别为-0.904,-0.900,-0.919及-0.895,P值皆小于0.01;能不同程度抑制心、肝、肾组织中SOD活力下降,其量效关系均呈正相关,r分别为0.983,0.973,0.968,P值皆小于0.01;能不同程度抑制心、肝、肾组织中GSH-PX活力下降,其量效关系均呈正相关,r分别为0.948,0.937,0.924,P值皆小于0.01。结论:中药祛癍方通过清除氧自由基和活性氧,提高抗氧化酶活性而发挥抗脂质过氧化作用。OBJECTIVE To observe the effects of the extract from a prescription of chinese medical herbs for eliminating senile plaque on malondialdehyde(MDA), superoxide dismutase(SOD) and glutathioneperoxidase(GSH-PX) in heart, liver and kidney and lipofuscin(LF) in brain of senile model mouce. METHODS MDA was measured by TBA colorimetric method. SOD was determined by nitrite method. GSH-PX was measured by DTNB method in heart,liver and kidney and LF was determined by Sohal method in brain of senile model mouce caused by D-galatose (D-gal) which were administered the extact through water from 3. 3,6. 5.13,26·g·kg^-1·d^-1 plant drugs on CMH once a day for 7 weeks respectively. RESULTS MDA content ascended.activities of SOD and GSH-PX droped in heart,liver and kidney, LF ascended in brain of senile model mice that caused by D-gal. But it differently resisted LF ascent in brain and MDA content ascent in heart,liver and kidney that senile model mouce were administrated respectively the extact through water from 3.3,6. 5,13.26 g·kg^-1·d^-1 plant drugs on CMH whose relation between quantity and efficiency showed all negative relativity. It differently inhibited activity-dropping of SOD and GSH-PX in heart,liver and kidney that senile mouce were administered the extract whose relation between quantity and efficiency showed all potive relativity. CONCLUSION The prescription exerts its effect on antilipoperoxidation by eliminating oxyen free radical-sand active oxyen, rising activities of antioxidases.
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