Abstract
Banhasasim-tang (BHS) is an herbal medicine that has been widely used in East Asia to treat various symptoms associated with upper abdomen swelling. BHS has not been studied previously for neuroinflammation or cognitive disorder. Here, we use a lipopolysaccharide (LPS) model to investigate the effects and mechanisms of BHS in neuroinflammation and cognitive impairment of mice. We used a mouse model of LPS-induced cognitive impairment and neuroinflammation and examined whether administration of BHS prevents these deficits via Morris water maze test, passive avoidance test, histopathological analysis, Western blotting, and real-time reverse transcription polymerase chain reaction (RT-qPCR). We found via behavioral tests that BHS treatment effectively prevented LPS-induced memory loss and neuronal damage in mice. Histopathological analysis of mouse brains revealed that BHS inhibited LPS-induced expression of microglial and astrocyte activation markers. Furthermore, BHS inhibits the production of markers related to neurodegeneration, amyloidogenesis, and inflammation, and mRNA expression of inflammatory mediators in mouse brain tissue. Additionally, BHS pretreatment effectively inhibited generation of inflammatory factors and pathways in BV2 microglial cells stimulated by LPS. These observations indicate that BHS is effective in preventing cognitive impairment caused by neuroinflammation and has strong potential as a candidate treatment for neuronal inflammatory diseases.
Highlights
Neuroinflammation is a reported part of the neuropathogenesis of cognitive impairment [1]
To determine the influence of BHS on LPS-induced memory loss, we performed an Morris water maze (MWM) test and measured the escape latency time and distance from the water maze in order to examine the ability of mice to learn their location and exhibit spatial memory recall
BHS is an important herbal medication that has long been used in East Asia; several of its beneficial pharmacological functions have been reported in recent studies, its effects on systemic inflammatory reactions or cognitive impairment have not been studied
Summary
Neuroinflammation is a reported part of the neuropathogenesis of cognitive impairment [1]. It is an important factor contributing to neurodegenerative diseases such as Alzheimer’s disease [2]. Microglia are extensively activated, promoting the production of inflammatory mediators that further lead to astrocyte activation and neuronal damage. TLR-4 is primarily expressed on macrophages and microglia, which, once activated, produce various inflammatory mediators [6,7]. These substances are key mediators of the neuroinflammatory process in the central nervous system (CNS). The injection of LPS into animals induces cognitive impairment and behavioral disorder including anorexia and Nutrients 2020, 12, 2019; doi:10.3390/nu12072019 www.mdpi.com/journal/nutrients
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