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Baicalin alleviates lipopolysaccharide-induced neuroglial activation and inflammatory factors activation in hippocampus of adult mice

Laboratory Animal Research 2020년 36권 1호 p.32 ~ 32
Shah Murad-Ali, 박동주, 강주빈, 김명옥, 고필옥,
소속 상세정보
 ( Shah Murad-Ali ) - Gyeongsang National University College of Veterinary Medicine Department of Anatomy
박동주 ( Park Dong-Ju ) - Gyeongsang National University College of Veterinary Medicine Department of Anatomy
강주빈 ( Kang Ju-Bin ) - Gyeongsang National University College of Veterinary Medicine Department of Anatomy
김명옥 ( Kim Myeong-Ok ) - Gyeongsang National University Division of Life Science and Applied Life Science
고필옥 ( Koh Phil-Ok ) - Gyeongsang National University College of Veterinary Medicine Department of Anatomy

Abstract


Baicalin is a natural flavonoid that exerts a variety of pharmaceutical effects such as anti-inflammatory and antioxidant. Lipopolysaccharide (LPS) is an endotoxin that releases inflammatory cytokines and induces inflammatory response. This study was investigated the anti-inflammatory mechanism of baicalin against LPS-induced inflammatory response in the hippocampus. Adult mice were randomly grouped into control, LPS-treated, and LPS and baicalin co-treated animals. LPS (250?μg/kg/day) and baicalin (10?mg/kg/day) were administered intraperitoneally for 7 consecutive days. We measured neuroglia cells activation and inflammatory factors activation using Western blot analysis and immunofluorescence staining techniques. Ionized calcium binding adaptor molecule-1 (Iba-1) and glial fibrillary acidic protein (GFAP) are widely used as microglia and astrocyte markers, respectively. LPS treatment increased Iba-1 and GFAP expression, while baicalin co-treatment attenuated this overexpression. Nuclear factor-kappa B (NF-κB) is a key mediator of inflammation. Baicalin co-treatment alleviated LPS-induced increase of NF-κB in the hippocampus. In addition, LPS treatment upregulated pro-inflammatory cytokines including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α). However, baicalin co-treatment prevented LPS-induced increases of IL-1β and TNF-α in the hippocampus. Results from the present study showed that baicalin suppresses LPS-induced neuroinflammation by regulating microglia and astrocyte activation and modulating inflammatory factors in the hippocampus. Thus, these results demonstrate that baicalin has neuroprotective effect by alleviates microglia and astrocyte activation and modulates inflammatory response by suppressing NF-κB expression in hippocampus with neuroinflammation caused by LPS.

키워드

Baicalin; Hippocampus; Lipopolysaccharide; Neuroinflammation

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