Abstract
The important immune cells in the brain are called microglia acting as the central junction between neuroinflammation and neurodegenerative diseases. In patients of cognitive disorders and Alzheimer’s disease (AD) animal models, amoebic morphology and inflammatory pathways are activated to release numerous cells in the inflammatory factors by active microglia. Dendrobium nobile Lindl. alkaloids (DNLA) are a kind of naturally extracted product that exhibits neuroprotective and anti-inflammatory activities. We previously reported that DNLA effectively inhibited NF-κB signal pathway in AD models. But how does DNLA exert antiinflammatory action is unknown. To study microglia-mediated inflammation, BV2 microglia cells were used to examine the effects of DNLA against LPS-induced inflammatory response. We found that DNLA reduced LPS-induced production of TNF-a and levels of Nlrp3 and IL-1ß mRNA, inhibited LPS-induced morphological changes, and decreased the protein expression of microglia marker Iba-1, inflammation-related factors iNOS in BV2 cells. Fortunately, DNLA significantly affected the expression of NF-κB p65, IκBa and their phosphorylative products in cellular nucleus and cytosol of LPS-induced BV2 microglia, and decreased TLR4, NLRP3, ASC, caspase-1, NEK7 and GSDMD expression of LPS-induced BV2 microglia. Taken together, the present study clearly demonstrated the protective effects of DNLA against LPS-induced inflammation in BV2 microglia, probably mediated through NF-κB and NLRP3 signaling pathways.
Keywords
Dendorbium Nobile Lindl. alkaloids, Lipopolysaccharide, Neurodegenerative diseases, BV2 microglia, NF-κB, NLRP3 inflammasome