Abstract
Lindera obtusiloba Blume (family, Lauraceae), native to Northeast Asia, has been used traditionally in the treatment of trauma and neuralgia. In this study, we investigated the neuroinflammatory effect of methanol extract of L. obtusiloba stem (LOS-ME) in a scopolamine-induced amnesia model and lipopolysaccharide (LPS)-stimulated BV2 microglia cells. LOS-ME downregulated the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase (COX)-2, inflammatory cytokines, and inhibited the phosphorylation of nuclear factor kappa-B (NF-ĸB) and extracellular signal-regulated kinase (ERK) in LPS-stimulated BV2 cells. Male C57/BL6 mice were orally administered 20 and 200 mg/kg of LOS-ME for one week, and 2 mg/kg of scopolamine was administered intraperitoneally on the 8th day. In vivo behavioral experiments (Y-maze and Morris water maze test) confirmed that LOS-ME alleviated cognitive impairments induced by scopolamine and the amount of iNOS expression decreased in the hippocampus of the mouse brain. Microglial hyper-activation was also reduced by LOS-ME pretreatment. These findings suggest that LOS-ME might have potential in the treatment for cognitive improvement by regulating neuroinflammation.
Highlights
Alzheimer’s disease (AD) is a progressive neurodegenerative disease with a wide range of clinical complications associated with memory loss and impairment of functional neurons leading to neuronal cell death [1,2]
To determine whether the decrease in nitric oxide (NO) production in BV2 microglia cells is due to the toxicity of BV2 microglia cells by L. obtusiloba stem (LOS)-ME, 3-(4,5-dimethylthiazol-2-yl)-2,5diphenyltetrazolium bromide (MTT) assay was performed
It is well documented that the inflammatory mediators in the central nervous system (CNS) causing neuroinflammation is one of the major pathogenic factors in neurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s disease (AD), Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS) [21,22,23,24]
Summary
Alzheimer’s disease (AD) is a progressive neurodegenerative disease with a wide range of clinical complications associated with memory loss and impairment of functional neurons leading to neuronal cell death [1,2]. Most cases of AD are late-onset and sporadic, with no proven evidence for a Mendelian pattern of inheritance. AD is characterized by impairments in hippocampal neurogenesis, associated cognitive dysfunction, and memory deficits [2]. The normal cholinergic system in the brain influences hippocampal neurogenesis and cognitive function by modulating neurogenic mechanisms such as those involving brain-derived neurotrophic factor (BDNF). Newly-formed neural progenitor cells at the dentate gyrus of the hippocampus grow as new functional neurons and integrate with the existing neuronal circuit, thereby act as crucial in cognition and memory [2]
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