香草酸通过抗氧化活性和抑制MPT孔开放减轻甲基苯丙胺诱导的心肌线粒体毒性:一项体外研究。

IF 2.8 3区 医学 Q2 PHARMACOLOGY & PHARMACY
Mohammad Shabani, Zhaleh Jamali, Deniz Bayrami, Ahmad Salimi
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引用次数: 0

摘要

背景:甲基苯丙胺在世界各地被广泛滥用。有报道称,短期和长期暴露于甲基苯丙胺会损害多巴胺能系统,并通过线粒体功能障碍和氧化应激诱发心肌病和心脏毒性。香草酸(VA)是一种从植物中提取的酚酸化合物,以其抗氧化和线粒体保护特性而闻名。方法:在本研究中,我们使用VA来减弱甲基苯丙胺对心脏线粒体的毒性。从大鼠心脏分离的线粒体分为:对照组,冰毒(250µM), VA(10、50和100µM)与冰毒(250µM)和VA(100µM)单独共处理。60 min后,测定线粒体部分,包括:琥珀酸脱氢酶(SDH)活性、线粒体膜电位(MMP)、线粒体肿胀、线粒体谷胱甘肽(GSH)、活性氧(ROS)和脂质过氧化(LPO)。结果:甲基苯丙胺暴露显著破坏线粒体功能,诱导ROS形成、脂质过氧化、GSH消耗、MMP塌陷和线粒体肿胀,而VA显著增加SDH活性,作为线粒体毒性和功能障碍的指标。在甲基苯丙胺存在下,VA还显著降低了ROS形成、脂质过氧化、线粒体肿胀、MMP塌陷和心脏线粒体GSH的消耗。结论:VA可减轻甲基苯丙胺诱导的线粒体功能障碍和氧化应激。我们的研究结果表明,VA可能通过抗氧化和线粒体保护特性,作为一种有前途的、可获得的抗甲基苯丙胺诱导的心脏毒性的心脏保护剂。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Vanillic acid alleviates methamphetamine-induced mitochondrial toxicity in cardiac mitochondria via antioxidant activity and inhibition of MPT Pore opening: an in-vitro study.

Vanillic acid alleviates methamphetamine-induced mitochondrial toxicity in cardiac mitochondria via antioxidant activity and inhibition of MPT Pore opening: an in-vitro study.

Vanillic acid alleviates methamphetamine-induced mitochondrial toxicity in cardiac mitochondria via antioxidant activity and inhibition of MPT Pore opening: an in-vitro study.

Vanillic acid alleviates methamphetamine-induced mitochondrial toxicity in cardiac mitochondria via antioxidant activity and inhibition of MPT Pore opening: an in-vitro study.

Background: Methamphetamine is widely abused in all parts of the world. It has been reported that short-term and long-term methamphetamine exposure could damage the dopaminergic system and induce cardiomyopathy and cardiotoxicity via mitochondrial dysfunction and oxidative stress. Vanillic acid (VA), a phenolic acid compound derived from plants, is known for its antioxidant and mitochondrial protection properties.

Methods: In the current study we used VA for attenuating of Methamphetamine-induced mitochondrial toxicity in cardiac mitochondria. Isolated mitochondria obtained from rat heart were grouped as: control, methamphetamine (250 µM), VA (10, 50 and 100 µM) was cotreated with methamphetamine (250 µM) and VA (100 µM) alone. After 60 min, mitochondrial fraction including: succinate dehydrogenases (SDH) activity, mitochondrial membrane potential (MMP), mitochondrial swelling, mitochondrial glutathione (GSH), reactive oxygen species (ROS) and lipid peroxidation (LPO) were evaluated.

Results: Methamphetamine exposure significantly disrupted mitochondrial function and induced ROS formation, lipid peroxidation, GSH depletion, MMP collapse and mitochondrial swelling, while VA significantly increased SDH activity as indicator of mitochondrial toxicity and dysfunction. VA also significantly decreased ROS formation, lipid peroxidation, mitochondrial swelling, MMP collapse and depletion of GSH in cardiac mitochondria in the presence of methamphetamine.

Conclusion: These findings suggested that VA is able to reduce methamphetamine-induced mitochondrial dysfunction and oxidative stress. Our results demonstrate that VA could potentially serve as a promising and accessible cardioprotective agent against methamphetamine-induced cardiotoxicity, via antioxidant and mitochondrial protection properties.

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来源期刊
BMC Pharmacology & Toxicology
BMC Pharmacology & Toxicology PHARMACOLOGY & PHARMACYTOXICOLOGY&nb-TOXICOLOGY
CiteScore
4.80
自引率
0.00%
发文量
87
审稿时长
12 weeks
期刊介绍: BMC Pharmacology and Toxicology is an open access, peer-reviewed journal that considers articles on all aspects of chemically defined therapeutic and toxic agents. The journal welcomes submissions from all fields of experimental and clinical pharmacology including clinical trials and toxicology.
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