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南蛇藤籽油对慢性铝诱导神经退行性变的皮质-海马挽救作用:神经行为学、生物化学、组织学研究

Cortico-hippocampal salvage in chronic aluminium induced neurodegeneration by Celastrus paniculatus seed oil: Neurobehavioural, biochemical, histological study.

作者信息

Chakrabarty Mrinmoy, Bhat Priyanka, Kumari Sweta, D'Souza Avin, Bairy K L, Chaturvedi Abhishek, Natarajan Archana, Rao Mohandas K G, Kamath Shobha

机构信息

Department of Pharmacology, Kasturba Medical College, Manipal, Karnataka, India.

出版信息

J Pharmacol Pharmacother. 2012 Apr;3(2):161-71. doi: 10.4103/0976-500X.95520.

Abstract

OBJECTIVE

To investigate the effects of Celastrus paniculatus seed oil in preventing the onset of chronic aluminum induced cortico-hippocampal neurodegeneration and oxidative stress.

MATERIALS AND METHODS

An animal model of senile dementia of Alzheimer's type was produced by administering aluminum as aluminum chloride (4.2 mg/kg) intraperitoneally to male Wistar rats for 60 days and results compared to untreated control. Neurobehavioral investigations of Morris water maze tests, passive avoidance test, rotarod test and biochemical estimations of acetylcholineterase, malondialdehyde, glucose-6-phosphate dehydrogenase, superoxide dismutase, and hemoglobin in blood were performed fortnightly which gauged the extent of global oxidative stress and progressive neural damage. Findings were fortified by the above enzyme assays and histology of brain at necropsy. Prophylactic oral C. paniculatus in two doses 0.5 ml and 1 ml, were given to animals and the results were analyzed in comparison to a similar rodent model with standard drug donepezil (0.5 mg/kg) intraperitoneally.

RESULTS

C. paniculatus showed a significant prevention in onset of aluminum induced neural insult and overall systemic oxidative stress which was corroborated by the enlisted neurobehavioral, biochemical, and histological evidence.

CONCLUSION

C. paniculatus is a putative decelerator of Al-mediated Alzheimer's like pathobiology.

摘要

目的

研究南蛇藤籽油对预防慢性铝诱导的皮质-海马神经退行性变和氧化应激发生的作用。

材料与方法

通过给雄性Wistar大鼠腹腔注射氯化铝(4.2毫克/千克)60天建立阿尔茨海默病型老年性痴呆动物模型,并将结果与未处理的对照组进行比较。每两周进行一次莫里斯水迷宫试验、被动回避试验、转棒试验的神经行为学研究以及血液中乙酰胆碱酯酶、丙二醛、葡萄糖-6-磷酸脱氢酶、超氧化物歧化酶和血红蛋白的生化测定,以评估整体氧化应激程度和进行性神经损伤。尸检时通过上述酶分析和脑组织学检查进一步证实研究结果。给动物口服两种剂量(0.5毫升和1毫升)的南蛇藤进行预防,并将结果与腹腔注射标准药物多奈哌齐(0.5毫克/千克)的类似啮齿动物模型进行比较分析。

结果

南蛇藤对铝诱导的神经损伤和整体全身氧化应激的发生有显著预防作用,这得到了所列举的神经行为学、生化和组织学证据的证实。

结论

南蛇藤可能是铝介导的类似阿尔茨海默病病理生物学的减速剂。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/26bd/3356958/2cd75f1b21d2/JPP-3-161-g001.jpg

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