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The effect of epicatechin on oxidative stress and mitochondrial damage induced by homocycteine using isolated rat hippocampus mitochondria

机译:表儿茶素对高半胱氨酸诱导的大鼠海马线粒体氧化应激和线粒体损伤的影响

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Oxidative stress and mitochondrial dysfunction are the main suggested mechanisms for neurodegenerative diseases. In this study, we have evaluated the effects of epicatechin (EC) on mitochondrial damage induced by homocycteine (Hcy) using isolated rat hippocampus mitochondria in vivo . EC (50 mg/kg) was gavaged daily for a period of 10 days, starting 5 days prior to Hcy (0.5 μmol/μL) intra hippocampus injection in rats. Mitochondria were isolated from brain by different centrifuge techniques. Mitochondrial function was assayed by MTT test. Also, mitochondrial swelling and oxidative stress markers, such as reactive oxygen species (ROS), lipid peroxidation and glutathione (GSH), were assayed. Hcy induced mitochondrial dysfunction and swelling. Increase in ROS formation, lipid peroxidation, and decreased GSH were observed after Hcy treatment in isolated brain mitochondria. Furthermore, oral administration of EC significantly decreased the lipid peroxidation and ROS levels and also increased GSH levels. Also, EC treatment significantly improved mitochondrial function. As EC indicated protective effects against oxidative stress and mitochondrial damage induced by Hcy, it is suggested for further trials for prevention or treatments of neurodegenerative disorders such as Alzheimer disease.
机译:氧化应激和线粒体功能障碍是神经退行性疾病的主要提示机制。在这项研究中,我们使用体内分离的大鼠海马线粒体评估了表儿茶素(EC)对高半胱氨酸(Hcy)诱导的线粒体损伤的作用。从大鼠海马内Hcy(0.5μmol/μL)注射前5天开始,每天灌胃EC(50 mg / kg),持续10天。通过不同的离心技术从大脑中分离出线粒体。通过MTT试验测定线粒体功能。此外,还测定了线粒体肿胀和氧化应激标记,例如活性氧(ROS),脂质过氧化和谷胱甘肽(GSH)。 Hcy引起线粒体功能障碍和肿胀。 Hcy治疗后,在孤立的脑线粒体中观察到ROS形成增加,脂质过氧化和GSH降低。此外,口服EC显着降低了脂质过氧化和ROS水平,还增加了GSH水平。而且,EC治疗显着改善了线粒体功能。由于EC指示对Hcy诱导的氧化应激和线粒体损伤具有保护作用,因此建议用于预防或治疗神经退行性疾病(例如阿尔茨海默氏病)的进一步试验。

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