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首页> 外文期刊>Daru Journal of pharmaceutical sciences. >An investigation of the neuroprotective effects of Curcumin in a model of Homocysteine - induced oxidative stress in the rat's brain
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An investigation of the neuroprotective effects of Curcumin in a model of Homocysteine - induced oxidative stress in the rat's brain

机译:姜黄素对同型半胱氨酸诱导的大鼠脑氧化应激模型的神经保护作用的研究。

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Background and the purpose of the studyAging is the major risk factor for neurodegenerative diseases and oxidative stress is involved in the pathophysiology of them. Oxidative stress can induce neuronal damages and modulate intracellular signaling, ultimately leading to neuronal death by apoptosis or necrosis. In this study, the possible antioxidant and neuroprotective properties of the natural polyphenolic antioxidant compound, curcumin against homocysteine (Hcy) neurotoxicity was investigated.MethodsCurcumin (5, 15, 45 mg/kg) was injected intraperitonealy (i.p.) once daily for a period of 10 days beginning 5 days prior to Hcy (0.2 μmol/μl) intracerebroventricular (i.c.v) injection in rats. Biochemical and behavioral studies, including passive avoidance learning and locomotor activity tests were studied 24 hrs after the last curcumin or its vehicle injection. The cell density of hippocampus layers and apoptosis in rats’ hippocampi by immunohistochical methods were also studied.Results and major conclusionResults indicated that Hcy could induce lipid peroxidation and increase Malondialdehyde (MDA) and Super Oxide Anion (SOA) levels in rat's brain. Additionally, Hcy impaired memory retention in passive avoidance learning test. However, curcumin decreased MDA and SOA levels significantly and improved learning and memory in rats. On the other hand Hcy could induce cell death and apoptosis in rats’ hippocampi which was inhibited by curcumin. These results suggest that Hcy may induce lipid peroxidation in rat's brain. and polyphenol treatment (curcumin) improves learning and memory deficits by protecting the nervous system against Oxidative stress.
机译:研究背景和目的衰老是神经退行性疾病的主要危险因素,氧化应激与它们的病理生理有关。氧化应激可诱导神经元损伤并调节细胞内信号传导,最终通过凋亡或坏死导致神经元死亡。在这项研究中,研究了天然多酚抗氧化剂化合物姜黄素对同型半胱氨酸(Hcy)神经毒性的可能的抗氧化和神经保护性能。方法腹膜内(ip)每天一次腹膜内注射姜黄素(5、15、45 mg / kg)从大鼠Hcy(0.2μmol/μl)脑室内(icv)注射前5天开始的10天。最后一次姜黄素或其媒介物注射后24小时,进行了生化和行为研究,包括被动回避学习和运动能力测试。结果和主要结论结果表明,Hcy可以诱导脂质过氧化,增加大鼠脑内丙二醛(MDA)和超氧阴离子(SOA)的含量。此外,Hcy会在被动回避学习测试中损害记忆力。然而,姜黄素可显着降低MDA和SOA水平,并改善大鼠的学习和记忆能力。另一方面,Hcy能诱导姜黄素抑制大鼠海马细胞死亡和凋亡。这些结果表明,Hcy可能会诱导大鼠大脑脂质过氧化。多酚治疗(姜黄素)通过保护神经系统免受氧化应激,改善学习和记忆障碍。

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