3-对氟苯甲酰丙酸对大鼠肝脏线粒体通透性、过渡开孔及脂质过氧化的体内外影响

A. Olowofolahan, Omosola L. Bolarin, O. Olorunsogo
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引用次数: 2

摘要

线粒体通透性转移(mPT)孔的打开是线粒体介导的细胞凋亡过程中一个公认的重要事件。一些生物活性化合物通过诱导mPT孔打开诱导肿瘤细胞凋亡。因此,本研究考察了氟哌啶醇代谢物3-对氟苯甲酰丙酸(3PFBPA)对mPT孔、线粒体atp酶活性(mATPase)、线粒体脂质过氧化(mLPO)和细胞色素c释放(CCR)的影响。将32只雄性Wistar大鼠置于洁净笼中驯化14 d。治疗30 d后处死,差速离心分离肝脏线粒体。用分光光度计测定mPT孔、mATPase、mLPO和CCR。3PFBPA诱导mPT孔开度分别为对照的1.4倍、3.6倍、5.6倍、6.6倍和7.4倍。此外,3PFBPA还能释放细胞色素c,增强mATPase活性。结果还表明,3PFBPA减少了脂质过氧化。与对照组相比,口服50、100和200 mg/kg的3PFBPA对mPT孔开度和mATPase活性没有影响,但对mLPO有抑制作用。这些发现表明,由于其抗脂质过氧化作用,3PFBPA具有抗细胞凋亡不足(基于体外数据)和氧化应激相关病理过程的药理潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
In vitro and in vivo effect of 3-Para-fluorobenzoyl-propionic acid on rat liver mitochondrial permeability transition pore opening and lipid peroxidation
Abstract The opening of mitochondrial permeability transition (mPT) pore is a well recognized important event in the execution of mitochondrial-mediated apoptosis. Some bioactive compounds induce apoptosis in tumour cells via the induction of mPT pore opening. This study therefore investigated the effect of 3-Para-fluorobenzoyl-propionic acid (3PFBPA), a metabolite of haloperidol on mPT pore, mitochondrial ATPase activity (mATPase), mitochondrial lipid peroxidation (mLPO) and cytochrome c release (CCR). Thirty-two male Wistar rats, were acclimatized for 14 days in clean cages. After 30 days of treatment, they were sacrificed and the liver mitochondria isolated using differential centrifugation. The mPT pore, mATPase, mLPO and CCR were determined by standard methods using a spectrophotometer. The mPT pore opening was induced by 3PFBPA by 1.4, 3.6, 5.6, 6.6 and 7.4 folds, when compared with the control. Also, there was release of cytochrome c and enhancement of mATPase activity by 3PFBPA. The results also show that 3PFBPA reduced lipid peroxidation. However, oral administration of 3PFBPA at 50, 100 and 200 mg/kg did not have any effect on mPT pore opening and mATPase activity when compared with the control but there was inhibition of mLPO. These findings suggested the pharmacological potential of 3PFBPA against the pathological processes related to insufficient apoptosis (based on the in vitro data) and oxidative stress due to its anti-lipidperoxidative effect.
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