Safavizadeh Naeimeh, Rahmani Seyed Ali, Zaefizadeh Mohamad
Department of Biology, Ahar Branch, IAU university, Ahar, Iran.
Indian J Hum Genet. 2013 Jan;19(1):18-25. doi: 10.4103/0971-6866.112879.
Multiple sclerosis (MS) is an autoimmune inflamatory disease, which affects the (Central Nervous System) and leads to the destruction of myelin and atrophy of the axons. Genetic factors, in addition to environmental ones, seem to play a role in MS. Numerous studies have reported mitochondrial defects including a reduction in cytochrome c oxidase (COX) complex function related to the reduction of mitochondrial genes expression in the cortex tissue of patients with MS have been reported.
This study aimed to assess COX5B and COX2 genes expression in MS patients and compare it with normal subjects. We determine expression levels of genes COX5B and COX2, and also gene reference ß-actine using real-time polymerase chain reaction (RT-PCR) method. Data were obtained and obtained and standardized with the gene reference and were analyzed using independent sample t-test with SPSS and Excel programs.
The resultshowed COX5B gene expression reduced significant in MS patients compared to normal subjects (P < -0.05) whereas, there was no significant difference in the COX2 gene expression between normal subjects and patients. Thus, it can be claimed that down-regulation of mitochondrial electron transport chain genes supported the hypothesis that hypoxia-like tissue injury in MS may be due to mitochondrial genes, different expression impairment.
多发性硬化症(MS)是一种自身免疫性炎症性疾病,会影响中枢神经系统,并导致髓鞘破坏和轴突萎缩。除环境因素外,遗传因素似乎也在MS中发挥作用。许多研究报告了线粒体缺陷,包括与MS患者皮质组织中线粒体基因表达减少相关的细胞色素c氧化酶(COX)复合物功能降低。
本研究旨在评估MS患者中COX5B和COX2基因的表达,并将其与正常受试者进行比较。我们使用实时聚合酶链反应(RT-PCR)方法测定COX5B和COX2基因以及基因参照β-肌动蛋白的表达水平。获取数据并用基因参照进行标准化处理,然后使用SPSS和Excel程序通过独立样本t检验进行分析。
结果显示,与正常受试者相比,MS患者中COX5B基因表达显著降低(P < -0.05),而正常受试者与患者之间COX2基因表达无显著差异。因此,可以认为线粒体电子传递链基因的下调支持了以下假设,即MS中类似缺氧的组织损伤可能是由于线粒体基因表达受损所致。