文献类型：期刊文献

英文题名：Antagonizing Effects of Soybean Isoflavones on ?-Amyloid Peptide-Induced Oxidative Damage in Neuron Mitochondria of Rats

作者：Feng, Jin-Fang[1];He, Ling-Ling[1];Li, Dan[2];Yuan, Lin-Hong[1];Yu, Huan-Ling[1];Ma, Wei-Wei[1];Yang, Yue[1];Xi, Yuan-Di[1];Ding, Juan[1];Xiao, Yi-Xiu[1];Xiao, Rong[1]

机构：[1]Capital Med Univ, Sch Publ Hlth & Family Med, Dept Nutr & Food Hyg, Beijing, Peoples R China;[2]E China Univ Sci & Technol, Shanghai 200237, Peoples R China

年份：2012

卷号：111

期号：4

起止页码：248

外文期刊名：BASIC & CLINICAL PHARMACOLOGY & TOXICOLOGY

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000308935000005)】；

基金：This work was supported by the grants from the National High Technology Research and Development Programme (863 Programme) of China (No. 2010AA023003), the National Natural Science Foundation of China (No. 30972470, 30771802) and the Funding Project for Academic Human Resources Development in Institutions of Higher Learning Under the Jurisdiction of Beijing Municipality (PHR201006112).

语种：英文

摘要：Soybean isoflavone (SIF) has been demonstrated to have neuroprotective effects induced by beta-amyloid peptides (A beta) through suppressing oxidative stress; however, the explicit mechanisms still remain uncovered. In the present study, 32 Wistar rats were randomly divided into four groups: an A beta 1-42-treated group, a SIF + A beta 1-42 group, a SIF-treated group and a control group. We measured the protein content of 8-hydroxydeoxyguanosine (8-OhdG) and mRNA expression of 8-oxoguanine DNA glycosylase (OGG1). The protein expression of OGG1, Bcl-xl, Bad, beta subunit of ATP synthase (ATPB) and pyruvate dehydrogenase (PDH) in brain was also measured. The results showed that the level of 8-OHdG in both SIF groups was significantly decreased compared to the A beta 1-42-treated group (p < 0.05), while the mRNA and protein expression of OGG1 in the SIF + A beta 1-42 groups were up-regulated compared with the A beta 1-42-treated groups (p < 0.05). The expression of Bcl-xl was up-regulated in the SIF-treated group compared with the A beta 1-42-treated groups (p < 0.05), while the expression of Bad was down-regulated in the two SIF-treated groups (p < 0.05). A beta 1-42 significantly down-regulated the expression of ATPase and PDH proteins compared with the control group (p < 0.05). SIF reversed the down-regulation effects on the mitochondrial energy metabolic enzymes induced by A beta 1-42 (p < 0.05) in the rats. These results suggest that SIF alleviate the oxidative stress in neurons and mitochondria of rat brains mediated by A beta 1-42, and these protective effects might be associated with the regulation of OGG1, Bad, Bcl-xl, ATPB and PDH.