【摘要】：目的觀察1-溴丙烷(1-BP)對大腦線粒體損傷和依達(dá)拉奉(EDA)的保護(hù)作用。方法將成年雄性Wistar大鼠隨機(jī)分為對照組、1-BP(800 mg/kg·bw)組、1-BP+1 mg/kg·bw EDA組、1-BP+3 mg/kg·bw EDA組、1-BP+5 mg/kg·bw EDA組、5 mg/kg·bw EDA對照組,每組12只。分別經(jīng)灌胃和腹腔注射給予1-BP和EDA,1次/d,連續(xù)12 d。動物處死后,迅速剝離大腦,采用差速離心法提取大腦前額葉皮層線粒體,檢測細(xì)胞線粒體復(fù)合體Ⅰ、Ⅱ、Ⅲ和Ⅳ活性;測定還原型谷胱甘肽(GSH)和氧化型谷胱甘肽(GSSG)含量,并計(jì)算GSH/GSSG比值;采用抗Neu N抗體進(jìn)行免疫組化染色,計(jì)數(shù)神經(jīng)元。結(jié)果 1-BP明顯降低大腦前額葉皮層細(xì)胞線粒體復(fù)合體Ⅰ、Ⅱ、Ⅲ、Ⅳ活性(P0.05,P0.01);1-BP組動物大腦皮層GSH含量也較對照組降低(P0.01),GSSG含量升高(P0.01),GSH/GSSG比值明顯降低(P0.01);給予1-BP染毒后,大腦前額葉皮層神經(jīng)元明顯減少(P0.01)。1-BP染毒同時(shí)給予不同劑量的EDA,大鼠大腦前額葉皮層線粒體復(fù)合體活性均有不同程度的升高;GSH含量降低也被明顯逆轉(zhuǎn),GSH/GSSG比值相應(yīng)升高(P0.05,P0.01);神經(jīng)元丟失明顯改善(P0.05,P0.01);EDA對1-BP誘導(dǎo)大腦損傷的保護(hù)作用呈現(xiàn)劑量-效應(yīng)關(guān)系(P0.05)。結(jié)論 1-BP導(dǎo)致大腦皮層線粒體損傷,腦內(nèi)氧化應(yīng)激及神經(jīng)元丟失,EDA可有效減輕1-BP神經(jīng)毒性。
[Abstract]:Objective to observe the protective effect of 1-bromopropane (1-BP) on cerebral mitochondria injury and Edaravone (EDA). Methods Adult male Wistar rats were randomly divided into control group, 1-BP (800 mg/kg bw) group, 1-BP 1 mg/kg bw EDA group, 1-BP 3 mg/kg bw EDA group and 1-BP 5 mg/kg bw EDA group. 5 mg/kg bw EDA control group, 12 rats in each group. 1-BP and EDA,1 were given intraperitoneally and intraperitoneally respectively for 12 days. After the animals were killed, the brain was rapidly stripped and the mitochondria of the prefrontal cortex were extracted by differential centrifugation. The activities of mitochondrial complexes 鈪，

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