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辅酶 Q10 对绝经后脊髓损伤大鼠模型 TNF-α、IL-10 水平及 Bax/Bcl2 比值的影响。

Coenzyme Q10 Influences on the Levels of TNF-α and IL-10 and the Ratio of Bax/Bcl2 in a Menopausal Rat Model Following Lumbar Spinal Cord Injury.

机构信息

Neuroscience Research Center (NRC), Iran University of Medical Sciences, Tehran, Iran.

Department of Anatomy, Faculty of Medicine, Iran University of Medical Sciences, Tehran, Iran.

出版信息

J Mol Neurosci. 2018 Jun;65(2):255-264. doi: 10.1007/s12031-018-1090-6. Epub 2018 Jun 14.

DOI:10.1007/s12031-018-1090-6
PMID:29948851
Abstract

The roles of the immune response and apoptosis as potential mediators of secondary damage in spinal cord injury (SCI) are being investigated. Research is also being done to determine the effects of female gonadal steroids, which decrease during menopause, and antioxidants, such as coenzyme Q10 (CoQ10) on SCI. We hypothesized that in the absence of female gonadal steroids, which provide protection following an SCI, CoQ10 could modulate the expression of cytokines, such as tumor necrosis factor (TNF)-α and interleukin (IL)-10, besides aquaporin-4 (AQP4) water channels in the CNS, which participate in neuroinflammation, as well as the Bax and Bcl2 proteins that are involved in apoptosis at the site of injury. The spinal cord was compressed at the level of the T10 vertebrae and rats were treated by 10 mg/kg/day CoQ10 for 3 weeks after surgery. The TNF-α and IL-10 expressions were studied using an ELISA. Western blot was used to investigate the Bax/Bcl-2 ratio, AQP4. The level of TNF-α significantly decreased following the administration of CoQ10 compared with the level of IL-10. When the treatment group was compared with the OVX-SCI group, the ratio of Bax/Bcl2 significantly decreased in the groups (P < 0.01). Based on our findings, CoQ10 could be used to compensate for the absence of the neuroprotection effects provided by female gonadal steroids via reducing the inappropriate effects of the two main pathways of secondary damage in SCI apoptosis.

摘要

正在研究免疫反应和细胞凋亡作为脊髓损伤 (SCI) 继发性损伤潜在介质的作用。还在研究女性性腺类固醇(在绝经期期间减少)和抗氧化剂(如辅酶 Q10 (CoQ10))对 SCI 的影响。我们假设,在缺乏女性性腺类固醇的情况下,后者可以在 SCI 后提供保护,CoQ10 可以调节细胞因子(如肿瘤坏死因子 (TNF)-α 和白细胞介素 (IL)-10)的表达,除了水通道蛋白-4 (AQP4) 水通道在中枢神经系统中参与神经炎症,以及参与损伤部位细胞凋亡的 Bax 和 Bcl2 蛋白。在 T10 椎骨水平压缩脊髓,并在手术后用 10mg/kg/天 CoQ10 治疗 3 周。使用 ELISA 研究 TNF-α 和 IL-10 的表达。使用 Western blot 研究 Bax/Bcl-2 比值、AQP4。与 IL-10 相比,CoQ10 给药后 TNF-α 的水平显着降低。与 OVX-SCI 组相比,治疗组的 Bax/Bcl2 比值显着降低(P<0.01)。根据我们的发现,CoQ10 可以通过减少 SCI 细胞凋亡中两个主要继发性损伤途径的不当作用来补偿女性性腺类固醇缺乏带来的神经保护作用。

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