Abstract
Angelicae Gigantis Radix (AGR) has been widely used as a traditional medicine in East Asia. The effects of AGR on neuroinflammation have not previously been studied in detail. In the study presented here, we investigated the antineuroinflammatory properties of this herb and its mechanism of operation. The effects of AGR on neuroinflammation were studied by measuring the production of inflammatory factors and related enzymes, and analyzing the expression levels of proteins and genes involved its activity, in lipopolysaccharide (LPS)-stimulated BV2 microglia. We found that AGR pretreatment strongly inhibits the production of nitric oxide (NO), cytokines, and the enzymes inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX)-2, and effectively induces the activation of heme oxygenase (HO)-1 and its regulator, nuclear factor erythroid 2-related factor 2 (Nrf-2). We also found that AGR effectively regulates the activation of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK). We confirmed the antineuroinflammatory effects of the main constituents of the plant as identified by high-performance liquid chromatography (HPLC). Our results indicate that the neuroinflammation inhibitory activity of AGR occurs through inhibition of NF-κB and MAPK and activation of Nrf-2.
Highlights
Neuroinflammation is one part of the immune reaction to harmful stimulation in the central nervous system
Our results indicate that the neuroinflammation inhibitory activity of Angelicae Gigantis Radix (AGR) occurs through inhibition of nuclear factor (NF)-κB and mitogen-activated protein kinase (MAPK) and activation of nuclear factor erythroid 2-related factor 2 (Nrf-2)
We investigated how the potency of the extracts correlated with the activation or inactivation of the NF-κB, MAPK, and Nrf-2 signaling pathways
Summary
Neuroinflammation is one part of the immune reaction to harmful stimulation in the central nervous system. The function of the neuroinflammatory response is to remove necrotic cells and tissues caused by pathogenic infections, disease, and other damage. Uncontrolled neuroinflammation, contributes to the progress of neurodegenerative diseases including Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease [1]. Microglial cells, brain-specific macrophages that reside in the central nervous system (CNS), play a critical role in maintaining the homeostasis of the brain and the neuroinflammatory response [2]. Microglia contribute to the maintenance of synaptic homeostasis by removing debris such as damaged neurons and pathogens from the central nervous system [3].
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