Effects of quercetin in preclinical models of Parkinson's disease: A systematic review

被引:0
|
作者
Vian, Camila de Oliveira [1 ,2 ,4 ]
Marinho, Marcelo Augusto Germani [1 ,2 ]
Marques, Magno da Silva [1 ,2 ]
Hort, Mariana Appel [1 ,2 ]
Cordeiro, Marcos Freitas [3 ]
Horn, Ana Paula [1 ,2 ]
机构
[1] Univ Fed Rio Grande FURG, Programa Posgrad Ciencias Fisiol, Rio Grande, Brazil
[2] Inst Ciencias Biol, Lab Neurociencias, FURG, Rio Grande, Brazil
[3] Univ Oeste Santa Catarina Unoesc, Programa Posgrad Biociencias & Saude, Joacaba, Brazil
[4] Fed Univ Rio Grande FURG, Lab Neurociencias, Inst Ciencias Biol, Av Italia,Km 8, BR-96210900 Rio Grande, RS, Brazil
关键词
flavonoids; neuroprotection; oxidative stress; Parkinson's disease; quercetin; ROTENONE RAT MODEL; GENE-EXPRESSION; MITOCHONDRIAL DYSFUNCTION; OXIDATIVE STRESS; CELLS; 6-OHDA; NEURODEGENERATION; NEUROTOXICITY; COMBINATION; INHIBITION;
D O I
10.1111/bcpt.14011
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Parkinson's disease (PD) is a neurodegenerative disease that affects dopaminergic neurons, thus impairing dopaminergic signalling. Quercetin (QUE) has antioxidant and neuroprotective properties that are promising for the treatment of PD. This systematic review aimed to investigate the therapeutic effects of QUE against PD in preclinical models. The systematic search was performed in PubMed, Scopus and Web of Science. At the final screening stage, 26 articles were selected according to pre-established criteria. Selected studies used different methods for PD induction, as well as animal models. Most studies used rats (73.08%) and mice (23.08%), with 6-OHDA as the main strategy for PD induction (38.6%), followed by rotenone (30.8%). QUE was tested immersed in oil, nanosystems or in free formulations, in varied routes of administration and doses, ranging from 10 to 400 mg/kg and from 5 to 200 mg/kg in oral and intraperitoneal administrations, respectively. Overall, evidence from published data suggests a potential use of QUE as a treatment for PD, mainly through the inhibition of oxidative stress, neuroinflammatory response and apoptotic pathways.
引用
收藏
页码:3 / 22
页数:20
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