Qi-activating quercetin alleviates mitochondrial dysfunction and neuroinflammation in vivo and in vitro
- PDF / 2,065,949 Bytes
- 14 Pages / 595.276 x 790.866 pts Page_size
- 40 Downloads / 170 Views
Online ISSN 1976-3786 Print ISSN 0253-6269
RESEARCH ARTICLE
Qi-activating quercetin alleviates mitochondrial dysfunction and neuroinflammation in vivo and in vitro Sora Kang1 · Ying Piao1,5 · Young Cheol Kang1 · Suyeol Lim2 · Youngmi Kim Pak1,2,3,4
Received: 8 November 2019 / Accepted: 19 May 2020 © The Pharmaceutical Society of Korea 2020
Abstract Parkinson’s disease (PD) is a multifactorial neurodegenerative disease manifesting mitochondrial damages and neuroinflammation. Qi is defined as a natural power that can regulate the energy flow in Oriental medicine, whereas mitochondria generate energy power in Western medicine. We investigated whether Qi-enhancing component in Oriental herb medicines could activate mitochondrial activities. Quercetin was found as a major bioactive compound in most Qi-activating Oriental herb medicines through online search for active compounds in several Oriental Medicine databases. We then investigated if quercetin could reverse 1-methyl-4-phenylpyridinium (MPP+)-induced mitochondrial dysfunction and lipopolysaccharide (LPS)-induced neuroinflammation. Mitochondrial activities were monitored based on complex 1 NADH dehydrogenase activities, ATP contents, mitochondrial membrane potential, cellular/mitochondrial reactive oxygen species, and oxygen consumption rate in SH-SY5Y cells. Quercetin at concentration up
to 20 µg/ml was not cytotoxic to SH-SY5Y cells. Pre-treatment with quercetin significantly protected mitochondrial damages in 1 mM M PP+- or 100 ng/ml LPS-treated cells. Quercetin increased expression levels of tyrosine hydroxylase and mitochondria controlling proteins. When in vivo effects of quercetin were assessed by immunohistochemical staining of tissue sections from LPS-injected mice brains, quercetin reduced the activation of microglia and astrocytes in the hippocampus and substantia nigra of LPS-injected mice. Our data suggest that Qi-activating quercetin might be therapeutically effective for neuroinflammation-mediated neurodegeneration by alleviating mitochondrial damages.
Electronic supplementary material The online version of this article (https://doi.org/10.1007/s12272-020-01238-x) contains supplementary material, which is available to authorized users.
Parkinson’s disease (PD) is a neurodegenerative disease characterized by selective loss of tyrosine hydroxylase (TH)-positive dopaminergic neurons in the substantia nigra (SN) (Obeso et al. 2010). Although causes of PD remain unclear, evidence strongly suggests that mitochondrial dysfunction and oxidative stress are involved in its pathogenesis (Moore et al. 2005; Henchcliffe and Beal 2008). Several PARK gene products associated with familial PD are present in mitochondrial membrane. They play important roles in maintaining fission and fusion of mitochondrial reticulum (Ebadi et al. 2001). Mutations in PARK genes and mitochondrial DNA have been found in the SN region of PD patients (Luoma et al. 2004). Notably, complex 1 (NADH-ubiquinone oxidoreductase) activity of mitochondrial oxidative phosphorylat
Data Loading...
