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Effect of coenzyme Q10 on mitochondrial respiratory proteins in trigeminal neuralgia

机译:辅酶Q10对三叉神经痛中线粒体呼吸蛋白的影响

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Trigeminal neuralgia (TN) is the neuropathic pain. Mitochondrial dysfunction, increased oxidative stress, and inflammation demonstrated in chronic pain. Carbamazepine (CBZ) is the first-line drug for TN, however, it is still insufficient. Coenzyme Q10 (CoQ10) has been used as the additional supplement for pain therapy. Nonetheless, mitochondrial respiratory proteins, oxidative stress, and inflammation in TN, and the add-on effects of CoQ10 on those defects have never been investigated. CBZ-treated TN-patients, na飗e TN-patients, and control subjects were included. CBZ-treated TN-patients were randomised into two subgroups, received either CoQ10 or placebo for 2 months. Pain levels were evaluated, and peripheral blood mononuclear cells were isolated to determine the oxidative stress, mitochondrial oxidative phosphorylation (OXPHOS), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1?, and cytokines including TNF-? IL-1?and IL-18 mRNA expression. Pain scales, oxidative stress, and OXPHOS levels were greater in na飗e TN-patients than control, whereas the cytokine profiles were unchanged. Although pain scales were lower in CBZ-treated TN-patients than in na飗e TN-patients, oxidative stress, OXPHOS, and cytokine expression profiles were not different. PGC-1?levels found to be increased in CBZ-treated TN patients when compared with the na飗e group. CoQ10 supplement in CBZ-treated TN patients reduced pain scale and oxidative stress and increased antioxidants levels when compared with placebo group. However, OXPHOS, PGC-1? and cytokines were not different between groups. These findings suggest that increased oxidative stress could be potentially involved in the pathogenesis of TN. CoQ10 supplements can reduce oxidative stress, leading to more effective pain reduction in TN patients being treated with CBZ. ?2018 Informa UK Limited, trading as Taylor & Francis Group.
机译:三叉神经痛(TN)是神经性疼痛。线粒体功能障碍,增加氧化应激和炎症,慢性疼痛。 Carbamazepine(CBZ)是TN的一线药物,但是,它仍然不足。辅酶Q10(COQ10)已被用作疼痛治疗的额外补充剂。尽管如此,从未研究过,在TN中的线粒体呼吸蛋白,氧化应激和氧化胁迫和CoQ10对这些缺陷的含量效果。包括CBZ治疗的TN患者,NA飗ETN患者和对照受试者。将CBZ处理的TN患者随机分为两种亚组,接受COQ10或安慰剂2个月。评估疼痛水平,分离外周血单核细胞,以确定氧化应激,线粒体氧化磷酸化(汤膦酸),过氧化物体增殖物激活的受体γ-α(PGC-1?,包括TNF-β1-1的细胞因子。 ?和IL-18 mRNA表达。疼痛尺度,氧化应激和毒药水平在Na e飗eTN患者中比对照更大,而细胞因子谱不变。虽然CBZ治疗的TN患者疼痛鳞片较低,但比在Na飗eTN患者,氧化应激,毒物和细胞因子表达谱不同。与Na e E组相比,CBZ处理的TN患者中发现的pGC-1?水平增加。COQ10补充CBZ治疗与安慰剂组相比,TN患者减少疼痛规模和氧化应激和抗氧化剂水平增加。然而,汤膦,PGC-1?和细胞因子在组之间没有差异。这些发现表明增加氧化应激可能是宝依据TN的发病机制。 CoQ10补充剂可以减少氧化应激,导致CBZ治疗的TN患者的更有效的疼痛减少。 ?2018年Informa UK Limited,贸易为泰勒和弗朗西斯集团。

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