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首页> 外文期刊>BioFactors >Bezafibrate induced increase in mitochondrial electron transport chain complex IV activity in human astrocytoma cells: Implications for mitochondrial cytopathies and neurodegenerative diseases
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Bezafibrate induced increase in mitochondrial electron transport chain complex IV activity in human astrocytoma cells: Implications for mitochondrial cytopathies and neurodegenerative diseases

机译：苯扎贝特诱导的人类星形细胞瘤细胞线粒体电子转运链复合物IV活性增加：对线粒体细胞病变和神经退行性疾病的影响

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Mitochondrial encephalomyopathies resulting from electron transport chain (ETC) dysfunction can present with a wide spectrum of clinical manifestations having significant neuropathology and a progressive nature. Despite advances in diagnosis of ETC disorders, treatment still remains inadequate. A recent study in fibroblasts and myoblasts revealed the ability of fibrate treatment to correct ETC enzyme deficiencies. Therefore, fibrates may represent potential therapeutic agents to correct the neurological ETC impairment responsible for the encephalopathic presentation of these disorders. Consequently, this study assessed the effect of bezafibrate on human astrocytoma (HA) 1321N cell ETC activity and coenzyme Q_(10) (CoQ_(10)) status. HA cells were incubated for 72 H with 300 μM or 500 μM bezafibrate and for 7 days with only 500 μM bezafibrate. A significant effect on ETC activity was observed after 7 days incubation with 500 μM bezafibrate yielding a 130% (P < 0.05) increase in complex IV activity, accompanied by a 33% (P < 0.05) increase in cellular ATP level and a 25% (P < 0.001) decrease in extracellular lactate/pyruvate ratio compared to control levels. Following 7 days culture with bezafibrate, the CoQ_(10) status of the HA cells appeared to increase although this was not found to be significant. The results of this study have indicated evidence of a bezafibrate induced increase in ETC complex IV activity. Further studies are required to assess the ability of bezafibrate treatment to correct neurological ETC impairment in available animal models of ETC dysfunction before the therapeutic efficacy of this pharmacological agent can be further considered in the treatment of the encephalopathic presentation of ETC disorders.
机译：由电子运输链（ETC）功能障碍导致的线粒体脑肌病可出现多种具有明显神经病理学和进行性的临床表现。尽管在ETC疾病的诊断方面取得了进步，但是治疗仍然不足。最近对成纤维细胞和成肌细胞的研究表明，纤维状药物治疗具有纠正ETC酶缺陷的能力。因此，贝特类药物可能代表潜在的治疗药物，以纠正造成这些疾病的脑病的神经ETC损伤。因此，本研究评估了苯扎贝特对人星形细胞瘤（HA）1321N细胞ETC活性和辅酶Q_（10）（CoQ_（10））状态的影响。 HA细胞与300μM或500μM苯扎贝特酸盐孵育72 H，仅与500μM苯扎贝特酸盐孵育7天。与500μM苯扎贝特孵育7天后，观察到对ETC活性有显着影响，复合物IV活性增加130％（P <0.05），同时细胞ATP水平增加33％（P <0.05）和25％与对照组相比，细胞外乳酸/丙酮酸盐比率降低（P <0.001）。用苯扎贝特培养7天后，HA细胞的CoQ_（10）状态似乎增加，尽管这并不重要。这项研究的结果表明，苯扎贝特诱导ETC复合物IV活性增加。需要进一步的研究来评估苯扎贝特治疗在可用的ETC功能障碍动物模型中纠正神经性ETC损伤的能力，然后才能在治疗ETC疾病的脑病性表现中进一步考虑该药理药物的治疗功效。

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