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Frontiers in Medical Science Research, 2023, 5(11); doi: 10.25236/FMSR.2023.051112.

Neuroprotective Effects of Fisetin by Fighting Neuroinflammation

Author(s)

Xiangwen Tang1,2, Peng Deng1,2, Hao Yang1,2

Corresponding Author:
Hao Yang
Affiliation(s)

1Shaanxi University of Chinese Medicine, Xianyang, Shaanxi, 712046, China

2Translational Medicine Center, Hong Hui Hospital Affiliated to Xi’an Jiaotong University, Xi’an, Shaanxi, 710054, China

Abstract

Neuroinflammation is an important event in the pathogenesis of most neurological diseases, whether acute, such as meningitis, brain trauma and stroke, or chronic, such as Parkinson's disease, Alzheimer's disease, and multiple sclerosis. A variety of factors, such as trauma, infection, metabolic abnormalities and autoimmune diseases, etc can cause it. Neuroinflammation is characterized by the activation of astrocytes and microglia and the production of inflammatory mediators. On the one hand, neuroinflammation can protect the body, mount defenses, support tissue repair and functional recovery. On the other hand, the neuroinflammatory cascade reactions lead to blood-brain barrier breakdown and apoptosis, ultimately contributing to the progression of the disease. Therefore, the search for a drug that inhibits neuroinflammation is crucial. In recent years, fisetin has attracted much attention due to its wide range of biological activities, including anti-aging, anti-inflammatory, antioxidant and anti-cancer. In particular, the anti-inflammatory potential of fisetin has led to its increasing research in the treatment of neurological disorders. This review summarizes fisetin's therapeutic benefits and mechanisms in neuroinflammation and its potential applications.

Keywords

Neuroinflammation; fisetin; microglia; astrocyte; anti-inflammatory

Cite This Paper

Xiangwen Tang, Peng Deng, Hao Yang. Neuroprotective Effects of Fisetin by Fighting Neuroinflammation. Frontiers in Medical Science Research (2023) Vol. 5, Issue 11: 79-85. https://doi.org/10.25236/FMSR.2023.051112.

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