Circulating Brain-Derived Neurotrophic Factor, Antioxidant Enzymes Activities, and Mitochondrial DNA in Bipolar Disorder: An Exploratory Report.

Circulating Brain-Derived Neurotrophic Factor, Antioxidant Enzymes Activities, and Mitochondrial DNA in Bipolar Disorder: An Exploratory Report.
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双相情感障碍中循环脑源性神经营养因子、抗氧化酶活性和线粒体 DNA:探索性报告。

DOI:
10.3389/fpsyt.2020.514658
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发表时间:
2020
影响因子:
4.7
通讯作者:
Chen X
Chen X
中科院分区:
医学3区
文献类型:
--
作者:
Wang D;Li H;Du X;Zhou J;Yuan L;Ren H;Yang X;Zhang G;Chen X

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积累的证据表明,神经营养蛋白失调、氧化应激损伤和线粒体功能障碍与双相情感障碍 (BD) 有关。然而,他们在 BD 中的真正作用尚不清楚。研究三个系统之间可能的交互对于理解这个复杂的过程是值得的。我们测量了 BD 患者 (n = 97) 和健康对照 (n = 31) 的血浆脑源性神经营养因子 (BDNF) 水平、白细胞线粒体 DNA 拷贝数 (mtDNAcn) 以及抗氧化酶活性。进行方差分析和线性回归分析来探讨 mtDNAcn、抗氧化酶和 BDNF 之间的相互作用。与健康对照相比,BD患者的谷胱甘肽过氧化物酶活性、BDNF水平和mtDNA含量显着降低,锰超氧化物歧化酶(MnSOD)活性显着升高(均p < 0.05)。回归分析显示 MnSOD 活性对 BDNF 有中等影响(β = 0.23,t = 8.5,p = 0.001)。抑郁症患者的铜锌 SOD 和总 SOD 活性与汉密尔顿抑郁量表评分显着相关(r = -0.38,p = 0.013;r = -0.35,p = 0.022)。出乎意料的是,我们观察到 BD 患者的 mtDNA 含量与 BDNF 之间没有显着相关性 (p > 0.05)。这些发现与我们的假设相一致,即异常的抗氧化酶、mtDNAcn 和外周 BDNF 可能参与 BD 的病程。外周BDNF、抗氧化酶活性和mtDNAcn之间存在显着相关性,提示氧化应激、线粒体功能和BDNF在BD中可能相互影响。
Accumulated evidence indicates that neurotrophin deregulations, oxidative stress injury, and mitochondrial dysfunction have been involved in bipolar disorder (BD); however, their real roles in BD are unclear. Investing the possible interaction between three systems is worthwhile understanding this complex process. We measured plasma brain-derived neurotrophic factor (BDNF) level, leukocytes mitochondrial DNA copy number (mtDNAcn), and activities of antioxidant enzymes in BD patients (n = 97) and healthy controls (n = 31). Analysis of variance and linear regression analyses were performed to explore the interaction between mtDNAcn, antioxidant enzymes, and BDNF. Compared with healthy controls, there were significant decreases of glutathione peroxidase activity, BDNF levels, and mtDNA content, significant increases of manganese superoxide dismutase (MnSOD) activity among BD patients (all p < 0.05). Regression analysis showed MnSOD activity had a moderate effect on BDNF (beta = 0.23, t = 8.5, p = 0.001). Copper zinc SOD and total SOD activity were significantly correlated with Hamilton Depression Scale scores in depressive patients (r = −0.38, p = 0.013; r = −0.35, p = 0.022). Unexpectedly, we observed no significant correlation between mtDNA content and BDNF in BD patients (p > 0.05). The findings coincide with our hypothesis that abnormal antioxidant enzymes, mtDNAcn, and peripheral BDNF may be involved in the course of BD. There were significant correlations between peripheral BDNF, antioxidant enzyme activities and mtDNAcn, suggesting that oxidative stress, mitochondrial function, and BDNF may influence each other in BD.
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