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Article ; Online: Magnesium Lithospermate B Suppresses Lipopolysaccharide-Induced Neuroinflammation in BV2 Microglial Cells and Attenuates Neurodegeneration in Lipopolysaccharide-Injected Mice.

Tai, Yaojun / Qiu, Yujiao / Bao, Zhicheng

Journal of molecular neuroscience : MN

2018  Volume 64, Issue 1, Page(s) 80–92

Abstract: ... lipopolysaccharide-induced neurodegeneration and microglial activation in the hippocampus of adult mice ... in this pathological process. Magnesium lithospermate B (MLB) is one of the major bioactive components of Radix ... with MLB could not only suppress lipopolysaccharide (LPS)-induced proliferation and morphological changes ...

Abstract Chronic inflammation in the brain plays a critical role in major neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), and multiple sclerosis (MS). Microglia, the resident macrophages and intrinsic components of the central nervous system (CNS), appear to be the main effectors in this pathological process. Magnesium lithospermate B (MLB) is one of the major bioactive components of Radix Salviae miltiorrhizae, which has been documented to protect neurons against multiple types of neuronal injury. However, its functions on microglia and the related neuroinflammation remain unknown. In the present study, BV2 microglial cells were used to assess the anti-neuroinflammatory capacity of MLB. Our data show that treatment with MLB could not only suppress lipopolysaccharide (LPS)-induced proliferation and morphological changes, but also interfere with cell cycle progression in BV2 cells. More strikingly, it attenuated the production of the inflammatory mediator nitric oxide (NO) and a panel of pro-inflammatory cytokine in LPS-stimulated BV2 cells, including tumor necrosis factor-α (TNF-α), interleukin (IL)-1α, IL-1β, and IL-6, and also promoted a phenotypic switch from the M1 to the M2 phenotype. Additionally, an in vivo study showed that the administration of MLB could ameliorate lipopolysaccharide-induced neurodegeneration and microglial activation in the hippocampus of adult mice. Mechanistically, MLB blocked the activation of the NF-κB pathway upon LPS stimulation, indicating that the effects of MLB on microglia may be mediated by the NK-κB pathway. These results suggest the therapeutic potential of MLB as a novel anti-inflammatory and microglia-modulating drug for neurodegenerative diseases.
MeSH term(s) Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Cell Differentiation ; Cell Line ; Drugs, Chinese Herbal/pharmacology ; Drugs, Chinese Herbal/therapeutic use ; Interleukins/metabolism ; Lipopolysaccharides/toxicity ; Macrophages/cytology ; Macrophages/drug effects ; Macrophages/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Microglia/drug effects ; Microglia/metabolism ; NF-kappa B/metabolism ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/etiology ; Nitric Oxide/metabolism ; Tumor Necrosis Factor-alpha/metabolism
Chemical Substances Anti-Inflammatory Agents ; Drugs, Chinese Herbal ; Interleukins ; Lipopolysaccharides ; NF-kappa B ; Tumor Necrosis Factor-alpha ; lithospermate B (122021-74-3) ; Nitric Oxide (31C4KY9ESH)
Language English
Publishing date 2018-01
Publishing country United States
Document type Journal Article
ZDB-ID 1043392-2
ISSN 1559-1166 ; 0895-8696
ISSN (online) 1559-1166
ISSN 0895-8696
DOI 10.1007/s12031-017-1007-9
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