H. Faramarzi, Saffari- Chaleshtori, S. Zolghadri, M. Beheshtroo, A. Faramarzi, S. M. Shafiee
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引用次数: 0
摘要
异烟肼是抗结核药物之一,可引起氧化应激、脑组织损伤和精神障碍等副作用。本研究旨在探讨三氧化二铁纳米颗粒给药对异烟肼诱导大鼠脑组织氧化应激参数的影响。选取成年雄性Wistar大鼠40只(200 ~ 250 g),随机分为不给药组和4个实验组。实验组动物分别腹腔注射生理盐水、异烟肼50 mg/kg、异烟肼50 mg/kg和铁2o3纳米颗粒0.2或0.4 mg/kg。用分光光度法测定脑组织匀浆中过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽- s -转移酶(GST)活性、谷胱甘肽(gSH)、丙二醛(mda)和总蛋白水平。结果表明,异烟肼处理组小鼠脑组织中Cat和gSt活性以及gSH和mda水平均高于对照组,而在0.2或0.4 mg/kg Fe 2o3纳米颗粒处理后,氧化应激参数恢复到对照组水平(P < 0.05)。与对照组相比,任何处理组的Sod活性均未发生变化。本研究表明,纳米氧化铁可抑制异烟肼致精神损伤大鼠脑组织氧化应激。
Ferric oxide nanoparticles administration suppresses isoniazid induced oxidative stress in the rat brain tissue
Isoniazid is one of the anti-tuberculosis therapeutic agents capable of causing side effects such as oxi dative stress, brain tissue damage and mental disorders. This study aimed to investigate the effect of ferric oxide (Fe 2 o 3 ) nanoparticles administration on isoniazid-induced oxidative stress parameters in rat brain tissue. Forty adult male Wistar rats (200–250 g) were randomly divided into a group with no treatment as control and four experimental groups. Animals of experimental groups received intraperitoneally for 12 days daily saline, 50 mg/kg of isoniazid, 50 mg/kg of isoniazid and 0.2 or 0.4 mg/kg Fe 2 o 3 nanoparticles accordingly. The activity of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), the level of glutathione (gSH), malondialdehyde (mda) and total protein were determined in brain tissue homogenates by spectrophotometric methods. It was shown that Cat and gSt activities, as well as gSH and mda levels in the brain tissue of animals in the isoniazid-treated group were increased compared with the control untreated group, while following the treatment with 0.2 or 0.4 mg/kg Fe 2 o 3 nanoparticles the studied oxidative stress parameters returned to the control level (P < 0.05). No changes in Sod activity in any of the treated groups were observed compared to the control. This study showed that the administration of ferric oxide nanoparti cles can suppress isoniazid-induced oxidative stress in the brain tissue of rats mentally damaged by isoniazid.