中外医疗
中外醫療
중외의료
CHINA FOREIGN MEDICAL TREATMENT
2014年
15期
35-36
,共2页
依达拉奉%脑出血%自由基%SOD%MDA
依達拉奉%腦齣血%自由基%SOD%MDA
의체랍봉%뇌출혈%자유기%SOD%MDA
Edaravone%Cerebral hemorrhage%Free radicals%SOD%MDA
目的:探讨依达拉奉对脑出血大鼠血肿周围脑组织SOD及MDA的影响。方法选SD大鼠90只,随机分成3组,每组30只,分别为假手术组、脑出血组及依达拉奉治疗组。将大鼠自体血注入尾状核制成脑出血模型;用黄嘌呤氧化法检测神经细胞SOD含量,改良的硫代巴比妥酸法测定MDA含量。结果脑出血组与假手术组比较SOD活性显著降低,而MDA含量增加(P<0.05),依达拉奉治疗组与脑出血组相比,神经细胞SOD含量明显增高(P<0.05),而MDA含量减低,差异有统计学意义(P<0.05)。结论依达拉奉具有清除自由基作用,该作用与增加细胞SOD含量,抑制脂质过氧化过程有关。
目的:探討依達拉奉對腦齣血大鼠血腫週圍腦組織SOD及MDA的影響。方法選SD大鼠90隻,隨機分成3組,每組30隻,分彆為假手術組、腦齣血組及依達拉奉治療組。將大鼠自體血註入尾狀覈製成腦齣血模型;用黃嘌呤氧化法檢測神經細胞SOD含量,改良的硫代巴比妥痠法測定MDA含量。結果腦齣血組與假手術組比較SOD活性顯著降低,而MDA含量增加(P<0.05),依達拉奉治療組與腦齣血組相比,神經細胞SOD含量明顯增高(P<0.05),而MDA含量減低,差異有統計學意義(P<0.05)。結論依達拉奉具有清除自由基作用,該作用與增加細胞SOD含量,抑製脂質過氧化過程有關。
목적:탐토의체랍봉대뇌출혈대서혈종주위뇌조직SOD급MDA적영향。방법선SD대서90지,수궤분성3조,매조30지,분별위가수술조、뇌출혈조급의체랍봉치료조。장대서자체혈주입미상핵제성뇌출혈모형;용황표령양화법검측신경세포SOD함량,개량적류대파비타산법측정MDA함량。결과뇌출혈조여가수술조비교SOD활성현저강저,이MDA함량증가(P<0.05),의체랍봉치료조여뇌출혈조상비,신경세포SOD함량명현증고(P<0.05),이MDA함량감저,차이유통계학의의(P<0.05)。결론의체랍봉구유청제자유기작용,해작용여증가세포SOD함량,억제지질과양화과정유관。
Objective To investigate the effect of edaravone on SOD and MDA in brain tissue around the hematoma of rats with cerebral hemorrhage. Methods 90 SD rats were chosen and randomly divided into 3 groups, control group, the cerebral hemor-rhage group and edaravone treatment group, respectively, each group of 30 rats. Cerebral hemorrhage model was made by injecting the autologous blood of rats into caudate nucleus. Xanthine oxidation method was used to detect the content of SOD in nerve cells, and improved thiobarbituric acid method was adopted to detect the MDA content. Results Compared with the control group, the SOD activity of the cerebral hemorrhage group decreased significantly, but MDA content increased (P<0.05); compared with the cerebral hemorrhage group, the SOD content in nerve cells of edaravone treatment group obviously increased, but MDA content de-creased, the difference was statistically significant (P<0.05). Conclusion Edaravone has the effect of scavenging free radicals, which is related to the increase of cellular SOD content and inhibition of the lipid peroxidation process.