地奥心血康对急性脑缺血的保护作用

Protective effect of di'ao xinxue kang against acute cerebral ischemia

目的:观察由野生草本植物薯芋科的黄山药根茎中提取的甾体总皂甙精制而成的纯中药制剂地奥心血康对急性脑缺血损伤的保护作用。方法:实验于2004-03/2005-05在河南科技大学医学院机能学实验室完成。①选用昆明种小鼠130只,雄性。脑指数测定:选用65只小鼠,随机分为5组,每组13只:模型组,尼莫地平组用生理盐水灌胃,0.2mL/10g,连续7d;尼莫地平组术前尾静脉注射尼莫地平0.02mg/g(由山东新华制药股份有限公司生产,批号0300123,剂量10mL/支);地奥心血康低、高剂量组分别按0.5,1mg/g剂量灌胃2.5,5.0g/L地奥心血康溶液(成分原薯蓣总皂甙,剂量100mg/粒,由成都地奥制药集团有限公司生产,批号2304057),连续7d;正常组未造模,灌胃等量生理盐水,连续7d。②第8天,除正常组外其余小鼠麻醉后,结扎双侧颈总动脉和迷走神经,造成小鼠急性脑缺血模型。小鼠死后,取全脑,并计算脑指数(脑质量/体质量×100%)。大脑匀浆超氧化物歧化酶、谷胱甘肽过氧化物酶活性及丙二醛含量测定:其余小鼠分组及给药同“脑指数测定”。将除正常组小鼠外的52只麻醉后,结扎双侧颈总动脉10min后再灌注30min,然后断头取大脑皮质,制成匀浆,羟胺氧化法测定超氧化物歧化酶活性;硫代巴比妥酸法测定丙二醛含量;并用DTNB法测定谷胱甘肽过氧化物酶含量。③组间计量资料比较采用t检验。结果:小鼠130只均进入结果分析。①小鼠脑指数:尼莫地平组、地奥心血康高剂量组明显低于模型组(P<0.01);模型组明显高于假手术组(P<0.01);地奥心血康低剂量组与模型组相近。②小鼠脑匀浆超氧化物歧化酶和谷胱甘肽过氧化物酶活性:尼莫地平组和地奥心血康高剂量组明显高于模型组(P<0.01),模型组明显低于假手术组(P<0.01)。③小鼠脑匀浆丙二醛含量:尼莫地平组和地奥心血康高、低剂量组明显低于模型组(P<0.01),模型组明显高于假手术组(P<0.01)。结论:地奥心血康在急性脑缺血损伤过程中,通过清除氧自由基、抗氧化、减少脂质过氧化、阻断Ca2+内流等作用,减轻脑细胞的损伤,对脑组织细胞起保护作用。

AIM： To study protective effect of di＇ao xinxue kang （DAXXK）, pure Chinese preparation made by steroid overall glucoside extracted from the genus wilding dioscorea on acute cerebral ischemia. METHODS： The experiment was completed in the Enginery Laboratory of Medical College of Henan University of Science and Technology from March 2004 to May 2005. ① Totally 130 Kunming male mice were selected in this study. Assay of cerebral indexes： Totally 65 mice were randomly divided into 5 groups with 13 in each group： model group, nimodipine group （Mice were perfused with 0.2 mL/10 g saline for 10 days, and injected into vein of tail with 0.02 mg/g nimodipine before operation. Nimodipine was provided by Shandong Xinhua Pharmaceutical Limited Company, batch number： 0300123, 10 mL/branch）, low and high dosage of DAXXK groups [Mice were perfused with 2.5 g/L （0.5 mg/g） and 5.0 g/L （1 mg/g） DAXXK solution respectively for 7 days. The component of DAXXK was primary dioscin with the dosage of 100 mg/pill and provided by Chengdu Di ＇ao Pharmaceutical Group Company Limited, batch number. 2304057], and normal group （Mice were not modeled but perfused with the same volume of saline for 7 days）.② On the 8^th day, mice except in normal group were anesthetized and ligated bilateral common carotid artery and pneumogastric nerve so as to establish models of acute ischemia. Mice were obtained the whole brain to calculate cerebral indexes （brain mass/body mass × 10%）. Homogenated superoxide dismutase （SOD）, activity of glutathione peroxidase （GSH-PX） and content of malondialdehyde （MDA）： Other rats were grouped and administrated according to assay of cerebral index. Totally 52 mice except normal group were anesthetized, ligated bilateral common carotid artery for 10 minutes, and perfused for 30 minutes. Heads of mice were cut to obtain cerebral cortex to make homogenate after 30 minutes. Activity of.SOD was assayed with hydroxylamine oxidation method; content of MDA was assayed with barbituric-acid method; content of GSH-PX was assayed with DTNB method. ③ Measurement data among groups were compared with t test. RESULTS： Totally 130 mice entered the final analysis.① Cerebral indexes： Those in nimodipine group and high dosage of DAXXK group were lower than those in model group （P 〈 0.01）, but in model group were higher than those in sham operation group （P 〈 0.01）, and those in low dosage of DAXXK group were similar to those in model group. ② Content of SOD and activity of GSH-PX： Those in nimodipine group and high dosage of DAXXK group were higher than those in model group （P 〈 0.01）, but in model group were lower than those in sham operation group （P〈 0.01）. ③ Content of MDA： That in nimodipine group, low and high dosage of DAXXK groups was lower than that in model group （P 〈 0.01）, but in model group was higher than that in sham operation group （P 〈 0.01）. CONCLUSION： DAXXK can relieve damage of cerebral cells and protect brain tissue through clearing oxygen-derived free radidicals, inhibiting oxidation, decreasing lipid peroxidation and blocking internal flow of Ca^2＋ during acute cerebral ischemic injury.