Neuroprotective Effects of Isoquercetin: An In Vitro and In Vivo Study

(Pages: 355-365)
Qingxiao Yang, M.M, 1Zhichen Kang, M.D., 2Jingze Zhang, M.M, 1Fuling Qu, M.M, 2Bin Song, M.M, 1,*
Neurosurgery Department, Second Hospital of Jilin University, Changchun City, Jilin Province, 130000, China
Rehabilitation Department, Second Hospital of Jilin University, Changchun City, Jilin Province, 130000, China
Neurosurgery Department, Second Hospital of Jilin University, Changchun City, Jilin Province, 130000, China
Rehabilitation Department, Second Hospital of Jilin University, Changchun City, Jilin Province, 130000, China
*Corresponding Address: Neurosurgery Department Second Hospital of Jilin University Changchun City Jilin Province 130000 China Email:15526859189m0@sina.cn
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Yang Qingxiao, Kang Zhichen, Zhang Jingze, Qu Fuling, Song Bin. Neuroprotective Effects of Isoquercetin: An In Vitro and In Vivo Study. Cell J. 2021; 23(3): 355-365.

Abstract

Objective

Alzheimer’s disease (AD) is considered a neurodegenerative disease that affects the cognitive function of elderly individuals. In this study, we aimed to analyze the neuroprotective potential of isoquercetin against the in vitro and in vivo models of AD and investigated the possible underlying mechanisms.

Materials and Methods

The experimental study was performed on PC12 cells treated with lipopolysaccharide (LPS). Reactive oxygen species (ROS), antioxidant parameters, and pro-inflammatory cytokines were measured. In an in vivo approach, Wistar rats were used and divided into different groups. We carried out the Morris water test to determine the cognitive function. Biochemical parameters, antioxidant parameters, and pro-inflammatory parameters were examined.

Results

The non-toxic effect on PC12 cells was shown by isoquercetin. Isoquercetin significantly reduced the production of nitrate and ROS, along with the altered levels of antioxidants. Isoquercetin significantly (P<0.001) down-regulated proinflammatory cytokines in PC12 cells treated with LPS. In the in vivo approach, isoquercetin- treated groups considerably showed the up-regulation in the latency and transfer latency time, as compared with AD groups. Isoquercetin significantly reduced Aβ-peptide, protein carbonyl, while enhanced the production of brain- derived neurotrophic factor (BDNF) and acetylcholinesterase (AChE). Isoquercetin significantly (P<0.001) reduced pro-inflammatory cytokines and inflammatory mediators, as compared with AD groups.

Conclusion

Based on the results, we may infer that, through antioxidant and anti-inflammatory systems, isoquercetin prevented neurochemical and neurobehavioral modifications against the model of colchicine-induced AD rats.