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The Protective Effect of Korean Red Ginseng Against Rotenone-Induced Parkinson’s Disease in Rat Model: Modulation of Nuclear Factor-κβ and Caspase-3

鱼藤酮 帕金森病 人参 药理学 传统医学 调制(音乐) 半胱氨酸蛋白酶3 医学 疾病 化学 细胞凋亡 内科学 生物化学 线粒体 程序性细胞死亡 物理 病理 替代医学 声学
作者
Mai A. Zaafan,Amr M. Abdelhamid,Sherine M. Ibrahim
出处
期刊:Current Pharmaceutical Biotechnology [Bentham Science Publishers]
卷期号:20 (7): 588-594 被引量:17
标识
DOI:10.2174/1389201020666190611122747
摘要

Korean red ginseng was reported to have many biological effects like the antioxidant and the anti-inflammatory activities. Oxidative stress and neuro-inflammation play major roles in the pathogenesis of Parkinson's disease (PD). The current study aimed to investigate the protective effects of ginseng on rotenone-induced PD in rats.Rats were randomly allocated into 4 groups: normal rats, rotenone control, ginseng+rotenone and ginseng only treated rats. The severity of PD was evaluated through locomotor activity perceived in the open field test, histological examination and immunohistochemical detection of amyloid-β in brain tissues, in addition to the biochemical assessment of tyrosine hydroxylase activity in brain tissues. Moreover, the following parameters were investigated for studying the possible mechanisms of ginseng neuroprotective effect: nuclear factor-κβ (NF-κβ), tumor necrosis factor-alpha (TNF-α), caspase- 3, lipid peroxides and reduced glutathione (GSH).Ginseng exhibited potent neuroprotective effect that was reflected upon the histopathological examination, marked improvement in the locomotor activity and through its ability to suppress the amyloid- β deposition in the cortex and striatum along with significant increase in the tyrosine hydroxylase activity. Ginseng successfully inhibited the NF-κβ inflammatory pathway in brain tissues beside the inhibition of other oxidative stress and inflammatory mediators. Furthermore, it exhibited antiapoptotic effect via the inhibition of caspase-3 expression.Ginseng could be a promising treatment in PD. It can suppress dopaminergic neuron degeneration through variable mechanisms mainly via inhibition of NF-κβ pathway in addition to inhibition of oxidative stress and apoptosis.

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