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Aqueous Extract from Fructus Mume Decreases NEUROINFLAMMATION

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초록

Lipopolysaccharide(LPS)-induced neuroinflammation is associated with the pathogenesis of Alzheimer’s disease(AD), which is a key factor underlying the generation of amyloid beta. Requirements for therapies of neurodegenerative diseases such as AD are not only consistent efficacy for long periods, but also the elimination of potential risks for hepatotoxicity. Thus, this study aimed to evaluate the effect of Frunus mume water extract (FME) on LPS-induced hippocampal damage associated with inflammatory signals. ICR male mice(n=30) were divided into three groups. The normal group remained untreated, LPS group (positive control) was stimulated to express LPS-induced hippocampus damage, and FME group(treatment) was stimulated to express LPS-induced hippocampal damage and administered FME at 40 mg/kg/day. Mouse brain tissues were tested by hematoxylin and eosin staining and immunohistochemistry following inflammation markers such as tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase(iNOS), and cyclooxygenase-2(COX-2). FME administered at 40 mg/kg/day for seven days in saline solution significantly reduced brain inflammation in the hippocampi of LPS-stimulated mice. Moreover, FME regulated the expression of inflammatory proteins such as TNF-α, iNOS and COX-2. Our data exhibits that FME attenuates neuroinflammation and damage in brains of LPS-stimulated mice. These findings suggest that FME is a potential therapeutic agent in treating neuroinflammation and recommend further testing on the matter.

Abstract

Lipopolysaccharide(LPS)-induced neuroinflammation is associated with the pathogenesis of Alzheimer’s disease(AD), which is a key factor underlying the generation of amyloid beta. Requirements for therapies of neurodegenerative diseases such as AD are not only consistent efficacy for long periods, but also the elimination of potential risks for hepatotoxicity. Thus, this study aimed to evaluate the effect of Frunus mume water extract (FME) on LPS-induced hippocampal damage associated with inflammatory signals. ICR male mice(n=30) were divided into three groups. The normal group remained untreated, LPS group (positive control) was stimulated to express LPS-induced hippocampus damage, and FME group(treatment) was stimulated to express LPS-induced hippocampal damage and administered FME at 40 mg/kg/day. Mouse brain tissues were tested by hematoxylin and eosin staining and immunohistochemistry following inflammation markers such as tumor necrosis factor-α (TNF-α), inducible nitric oxide synthase(iNOS), and cyclooxygenase-2(COX-2). FME administered at 40 mg/kg/day for seven days in saline solution significantly reduced brain inflammation in the hippocampi of LPS-stimulated mice. Moreover, FME regulated the expression of inflammatory proteins such as TNF-α, iNOS and COX-2. Our data exhibits that FME attenuates neuroinflammation and damage in brains of LPS-stimulated mice. These findings suggest that FME is a potential therapeutic agent in treating neuroinflammation and recommend further testing on the matter.

참고문헌 (13)

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