Anti-inflammatory and neuroprotective effects of kissoone B and extracts of Valeriana amurensis
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ORIGINAL ARTICLE
Anti-inflammatory and neuroprotective effects of kissoone B and extracts of Valeriana amurensis Junkai Wu 1,2
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Jianping Guo 2
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Xiaowei Du 1
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Patrick L. Mcgeer 2
Received: 16 October 2019 / Accepted: 3 December 2020 / Published online: 8 September 2020 # Sociedade Brasileira de Farmacognosia 2020
Abstract Extracts of the roots and rhizomes of Valeriana amurensis P. Smirn. ex Kom., Caprifoliaceae, and kissoone B have shown a potential effect on neurological disorders in the past. We researched the anti-inflammatory effects and cell protective function of kissoone B and extracts of V. amurensis by the standard lactate dehydrogenase release test, and 3-(4,5-dimethylthiazol-2-yl)2,5diphenyl tetrazolium bromide survival assay. We also studied the effects of kissoone B and extracts of V. amurensis on γaminobutyric acid content in astrocytes Dulbecco’s Modified Eagle Medium/F12 medium. The petroleum ether part increased extracellular γ-aminobutyric acid concentration significantly, and kissoone B displayed about 60% effect of the petroleum ether part, close to the γ-aminobutyric acid release of ethyl acetate part. Then, the petroleum ether part of V. amurensis was administered to mouse, and γ-aminobutyric acid concentration in the mouse brain was determined. Γ-aminobutyric acid level in the mouse brain was increased significantly after administration of the petroleum ether part of V. amurensis. The water residue fraction protected cells and the purified fraction may have a potential treatment for neurological diseases, especially Alzheimer disease. Keywords Anti-inflammatory . THP-1 cells . SH-SY5Y cells . U373 cells . Lactic dehydrogenase . MTT assay
Introduction Alzheimer’s disease (AD) is an age-related neurodegenerative disease characterized by accumulation of Aβ and neurofibrillary tangles (Yuan and Yankner 2000). Although the etiology of AD remains unclear, a number of hypotheses have been proposed to explain the pathogenesis of AD, such as the amyloid hypothesis, inflammation hypothesis, and oxidative stress hypothesis (McGeer et al. 2006; Butterfield et al. 2007). For present, two classes of drugs have been approved to treat AD: acetylcholinesterase inhibitors, such as tacrine, donepezil, galantamine, and rivastigmine, and an N-methyl* Xiaowei Du [email protected] * Patrick L. Mcgeer [email protected] 1
Key laboratory of Chinese Materia Medica, Ministry of Education, Pharmaceutical College, Heilongjiang University of Chinese Medicine, Harbin, China
2
Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, Canada
D-aspartate
receptor antagonist, memantine. However, there currently is no effective treatment that delays the onset or slows the progression of AD, thus, how to prevent and cure AD becomes a difficult problem (Atri 2011). GABA is known as the main inhibitory neurotransmitter in the brain, and its exclusive function is believed in the CNS. For GABAergic cells human astrocytes and GABAceptive cells human microglia, GABA suppresses the res
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