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SO2体内衍生物对子鼠发育中肝和脑抗氧化功能与肝Bax免疫组化的影响

Effect of SO2 Derivatives on Antioxidant Function in the Liver and Brain and Bax Immunohistochemical in the Liver during Filial Mice Development

【作者】 尚建科

【导师】 俞诗源;

【作者基本信息】 西北师范大学 , 细胞生物学, 2008, 硕士

【摘要】 为探究SO2体内衍生物对子鼠发育过程中肝和脑的影响,以昆明小鼠为实验材料,以不同剂量SO2体内衍生物腹腔注射到孕鼠体内,检测了子鼠胚胎第15日、出生第1日和出生第10日肝和脑的SOD活性、MDA含量、GSH-PX活性、GSH含量,并且用免疫组化技术和体视学半定量方法研究了Bax在子鼠胚胎第15日、出生第1日和出生第10日肝脏中表达的面密度,然后用Excel和SPSS 13.0对SOD活性、MDA含量、GSH-PX活性、GSH含量和免疫组化面密度进行统计分析。结果如下:1.孕鼠腹腔注射SO2体内衍生物后,子鼠在胚胎第15日,注射SO2体内衍生物组肝和脑SOD活性比对照组SOD活性显著增高,但随发育持续,对照组子鼠肝和脑SOD活性增强,而注射SO2体内衍生物组子鼠肝和脑SOD活性下降,至出生后第10日,注射SO2体内衍生物组肝和脑SOD活性比对照组肝和脑SOD活性有极显著性下降。2.孕鼠腹腔注射SO2体内衍生物后,子鼠在胚胎第15日,注射SO2体内衍生物组随剂量增大肝和脑MDA含量降低,但随发育持续,对照组子鼠肝和脑MDA含量急剧减少,至出生第10日,注射SO2体内衍生物中剂量组子鼠肝和脑MDA含量有极显著性增加。3.孕鼠腹腔注射SO2体内衍生物后,子鼠在胚胎第15日时,注射SO2体内衍生物的中剂量组肝GSH-PX活性比对照组的肝GSH-PX活性有显著性增强,但随发育持续,对照组GSH-PX活性不断增强,但中剂量组GSH-PX活性减弱,至出生第10日时,中剂量组的肝GSH-PX活性比对照组的肝GSH-PX活性有极显著性减弱。4.孕鼠腹腔注射SO2体内衍生物后,子鼠在胚胎第15日时,注射二氧化硫体内衍生物的中剂量组肝GSH含量比对照组肝GSH含量比有极显著性减少,随发育持续,中剂量组GSH含量急剧增加,对照组GSH含量缓慢增加,至出生第10日时,低剂量组和中剂量组的肝GSH含量均比对照组有极显著性增多;子鼠在胚胎第15日时,注射SO2体内衍生物的中剂量脑GSH含量比对照组的脑GSH含量有极显著性增加,随发育持续,中剂量组GSH含量缓慢增加,对照组GSH含量迅速增加,至出生第10日时,低剂量组和中剂量组的脑GSH含量均比对照组有极显著性减少。5.孕鼠腹腔注射SO2体内衍生物后,子鼠在胚胎第15日时,注射SO2体内衍生物的中剂量组肝Bax免疫组化面密度比对照组的肝Bax免疫组化面密度有显著性增强,但随发育进行,对照组肝组织中Bax免疫组化面密度先增多后减少,用药组肝组织中Bax免疫组化面密度呈下降的趋势,至出生第10日时,中剂量组的肝Bax免疫组化面密度与对照组的肝Bax免疫组化面密度无显著性差异。表明孕鼠腹腔注射SO2体内衍生物会对子鼠发育过程中肝和脑的SOD活性有损伤作用;使子鼠发育过程中肝和脑的脂质过氧化水平升高;使子鼠发育过程中肝的GSH-PX活性降低;使子鼠发育过程中肝中GSH积累,使脑中GSH含量减少;使子鼠肝组织的Bax免疫组化面密度增大,但随发育持续这种影响减弱。证明SO2体内衍生物影响子鼠发育中肝和脑的抗氧化能力和肝脏的细胞凋亡过程。

【Abstract】 Sulfur dioxide derivatives divided into different dosage groups were injectedintraperitoneally into the pregnant mice in order to study that sulfur dioxide derivativeseffect on liver and brain during development of the filial mice. The activity of SOD,content of MDA, activity of GSH-PX and content of GSH in livers and brains atembryobic day 15, postnatal day 1 and postnatal day 10 were detected, and the surfacearea density of Bax expression in livers at embryobic day 15, postnatal day 1 andpostnatal day 10 were studied by immunohistochemical technique combined withsterological methods. The data were analyzed by statistical software SPSS 13.0 andExcel. The results were as follows.1. After sulfur dioxide derivatives were injected intraperitoneally into thepregnant mice, the activity of SOD in livers and brains of the treated groups weresignificantly higher than that of the control group at the 15th day embryo of the filialmice. However, during the following development, the SOD activity in livers andbrains of the control group increased gradually, while the SOD activity in livers andbrains of the treated groups decreased gradually. The SOD activity in livers and brainsof the treated groups were significantly lower than that of the control group at postnatalday 10.2. After sulfur dioxide derivatives were injected intraperitoneally into thepregnant mice, the content of MDA in livers and brains of the treated groups were veryless than that of the control group at the 15th day embryo of the filial mice. However,the MDA content in livers and brains of the control group decreased gradually duringthe following development. The MDA content in livers and brains of the treated groupswere very higher than that of the control group at postnatal day 10.3. After sulfur dioxide derivatives were injected intraperitoneally into thepregnant mice, the activity of GSH-PX in livers of the treated groups weresignificantly higher than that of the control group at the 15th day embryo of the filialmice. However, during the following development, the GSH-PX activity in livers ofthe control group increased gradually, while the GSH-PX activity in livers of the treated groups decreased gradually. The GSH-PX activity in livers of the treated groupswere very lower than that of the control group at postnatal day 10.4. After sulfur dioxide derivatives were injected intraperitoneally into thepregnant mice, the content of GSH in livers of the treated groups were very less thanthat of the control group at the 15th day embryo of the filial mice. However, during thefollowing development, the GSH content in livers of the treated group increasedgradually. The GSH content in livers of the treated groups were more than that of thecontrol group at postnatal day 10. At the 15th day embryo of the filial mice, the contentof GSH in brains of the medium-dose experimental groups were more than that of thecontrol group. However, during the following development, the GSH content in brainsof the control group increased gradually, the GSH content in brains of the controlgroups were more than that of the treated group at postnatal day 10.5. After sulfur dioxide derivatives were injected intraperitoneally into thepregnant mice, the surface area density of Bax expression in livers of the treatedgroups were significantly higher than that of the control group at the 15th day embryoof the filial mice. However, during the following development, the surface area densityof Bax expression in livers of the treated groups decreased gradually. there were nosignificant difference between the treated groups and the control group in surface areadensity of Bax expression in livers at postnatal day 10..The results were showed that: the activities of SOD in livers and brains wereinjuryed during development of the filial mice; lipid peroxidation level of livers andbrains were increased during development of the filial mice; the activities of GSH-PXin livers were injuryed during development of the filial mice; the content of GSH inlivers were increased during development of the filial mice, while the content of GSHin brains decreased; the surface area density of Bax expression in livers were increasedsignificantly at the 15th day embryo of the filial mice, but the influences wereweakening during the following development of the filial mice. It was proved thatsulfur dioxide derivaties influenced on antioxidant function in livers and brains andcell apoptosis activity in livers during the filial mice development.

【关键词】 二氧化硫小鼠抗氧化Bax
【Key words】 sulfurdioxidederivativesmiceliverbrainantioxidationBax
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