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5,6,7 trihydroxy flavone armoured neurodegeneration caused by Quinolinic acid induced huntington’s like disease in rat striatum - reinstating the level of brain neurotrophins with special reference to cognitive-socio behaviour, biochemical and histopathological aspects
Neuroscience Research ( IF 2.9 ) Pub Date : 2021-08-18 , DOI: 10.1016/j.neures.2021.08.003
Bhagyalakshmi Purushothaman 1 , Thangarajan Sumathi 1
Affiliation  

Huntington Disease (HD), a predominant Neurodegenerative Disorder which might be induced by endogenous neurotoxin called Quinolinic Acid (QA), an N-methyl-D aspartate receptor (NMDAR) agonist, the bilaterally intrastriatal administration (200 nm/2 μL of saline) offers rise to the toxic events like neuronal death, neuroinflammation by inflicting excitotoxicity and oxidative stress in the striatum of male Wistar rats by exhibiting the behavioural changes which was accessed by rotarod, open field analysis. In this study, the neuropharmacological effect of Baicalein (BC) against QA induced HD was evaluated. Baicalein (BC), scientifically 5,6,7 trihydroxy flavone present naturally in the edible plants like Scutellaria baicalensis and Oroxylum indicum possess a better neuroprotective effect in the dosage of 10 mg/kg and 30 mg/kg intraperitoneally in the striatum of HD induced rats. This study proved that BC is efficient to revive the level of enzymatic & non-enzymatic antioxidants and mitochondrial complexes by decreasing the number of inflammatory mediators such as MDA, protein carbonyls and Nitric Oxide at the significance of P < 0.01 and restores the amount of BDNF and GDNF thereby preventing the neurophysiological changes which were analysed by haematoxylin & eosin staining. Thus finally, the protective effect of Baicalein displays the up-gradation of psychological and behavioural changes induced by QA.



中文翻译:

5,6,7 三羟基黄酮装甲神经退行性变由喹啉酸诱导大鼠纹状体亨顿氏样疾病 - 恢复脑神经营养因子水平,特别参考认知 - 社会行为,生化和组织病理学方面

亨廷顿病 (HD),一种主要的神经退行性疾病,可能由称为喹啉酸 (QA) 的内源性神经毒素诱导,一种 N-甲基-D 天冬氨酸受体 (NMDAR) 激动剂,双侧纹状体内给药(200 nm/2 μL 盐水)通过展示通过旋转棒、开放场分析获得的行为变化,通过在雄性 Wistar 大鼠的纹状体中造成兴奋性毒性和氧化应激,从而引发毒性事件,如神经元死亡、神经炎症。在这项研究中,评估了黄芩素 (BC) 对 QA 诱导的 HD 的神经药理作用。黄芩素 (BC),科学 5,6,黄芩、黄芩等可食植物中天然存在的7种三羟基黄酮在10mg/kg和30mg/kg的剂量下对HD诱导大鼠纹状体腹腔内具有较好的神经保护作用。本研究证明 BC 通过减少炎症介质(如 MDA、蛋白质羰基和一氧化氮)的数量(P < 0.01)有效地恢复酶促和非酶促抗氧化剂和线粒体复合物的水平,并恢复 BDNF 的量和 GDNF 从而防止通过苏木精和伊红染色分析的神经生理学变化。因此,最后,黄芩素的保护作用显示了由 QA 引起的心理和行为变化的升级。本研究证明 BC 通过减少炎症介质(如 MDA、蛋白质羰基和一氧化氮)的数量(P < 0.01)有效地恢复酶促和非酶促抗氧化剂和线粒体复合物的水平,并恢复 BDNF 的量和 GDNF 从而防止通过苏木精和伊红染色分析的神经生理学变化。因此,最后,黄芩素的保护作用显示了由 QA 引起的心理和行为变化的升级。本研究证明 BC 通过减少炎症介质(如 MDA、蛋白质羰基和一氧化氮)的数量(P < 0.01)有效地恢复酶促和非酶促抗氧化剂和线粒体复合物的水平,并恢复 BDNF 的量和 GDNF 从而防止通过苏木精和伊红染色分析的神经生理学变化。因此,最后,黄芩素的保护作用显示了由 QA 引起的心理和行为变化的升级。01 并恢复 BDNF 和 GDNF 的数量,从而防止通过苏木精和伊红染色分析的神经生理学变化。因此,最后,黄芩素的保护作用显示了由 QA 引起的心理和行为变化的升级。01 并恢复 BDNF 和 GDNF 的数量,从而防止通过苏木精和伊红染色分析的神经生理学变化。因此,最后,黄芩素的保护作用显示了由 QA 引起的心理和行为变化的升级。

更新日期:2021-08-18
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