Abstract
The root of Saposhnikovia divaricata (Fangfeng) is commonly used in traditional Chinese medicine (TCM) for headache and neuroinflammation-related disease treatment. The mRNA expression of IL-6 and IL-1β were significantly inhibited after Fangfeng extract (FFE) treatment in LPS-induced BV-2 cells. Metatolome profiling indicated that dopamine, palmitic acid, corticosterone, and eicosapentaenoic acid metabolites could be regulated by FFE for LPS stimulated inflammation responses in BV-2 cells. The disturbed metabolic pathways include caffeine metabolism, mannose type O-glycan biosynthesis, arachidonic acid metabolism, and steroid biosynthesis. This study will enable us to identify potential protein targets and metabolite intermediates for FFE exerting its protective function in BV-2 cells, and it also provided a potential application of Fangfeng in neuroinflammation-related disease treatment.
Highlights
Many neuronal diseases might be activated by inflammatory processes and their specific mediators [1]
The fibrillar Aβ could induce microglial activation and cytokines secretion with AD compared with healthy controls [3]. α-synucein might activate inflammatory responses and induce IL-1β release and NLRP3 expression in a PD animal model [4]
Fangfeng is extensively applied in traditional Chinese medicine (TCM) for treating headaches, joint pain, and rheumatic arthritis [9]
Summary
Many neuronal diseases might be activated by inflammatory processes and their specific mediators [1]. The mutant huntingtin resulted in hyperinflammatory microglia and activated the key myeloid transcription factors Pu. and C/EBP (CCAAT/Enhancer Binding Protein) in microglia [5]. In this perspective, neuroinflammation cascade could be crucial for neurodegenerative diseases. Through traditional Chinese medicine and biological experiments, we speculate that Fangfeng may exert neuroprotective functions through attenuating neuroinflammation processes. Inhibition of the microglia-mediated neuroinflammatory response may be a potential treatment for neurodegenerative diseases [18]. Metabolomics has been widely applied to study the pharmacological mechanism of TCM, including the mechanism of TCM in treating neurodegenerative diseases [21]. We attempted to conduct an untargeted metabolomics investigation to disclose the potential and molecular mechanism of FFE for neuroinflammation protection
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