Vitamin D2 suppresses amyloid-β 25–35 induced microglial activation in BV2 cells by blocking the NF-κB inflammatory signaling pathway

    loading  Checking for direct PDF access through Ovid


Aims:Present emerging world is emphasizing the implication of vitamin D deficiency associated with development of inflammation and neurodegenerative disorder like Alzheimer's disease (AD). The chief neuropathological hallmark of AD is aggregation of amyloid-beta (Aβ) peptides surrounding microglial cells in human brain. Microglial activation plays a key role in inflammatory response and neuronal injury. Naturally abundant vitamin D2 (VD2) exhibiting anti-inflammatory activities are yet to explore more. This study has investigated the inhibitory effect of VD2 on inflammatory activities of BV2 microglial cells.Main methods:Cellular compatibility of VD2 and Aβ25–35 protein in treated BV2 microglial cells were measured by CCK-8 assay. Induction of iNOS, COX-2 and NF-κB signaling cascade were measured by western blotting, whereas pro-inflammatory cytokines were measured by ELISA. In addition, generation of ROS was detected by fluorescence intensity.Key findings:Morphological observations showed that Aβ25–35 induced BV2 cells stimulation noticeably got reduced in VD2 pre-treated group at 24 h time period. Anti-inflammatory activities of VD2 was observed demonstrating the inhibition of up-regulated iNOS and COX-2 protein expression further confirmed by attenuating the activated microglia released pro-inflammatory cytokines IL-1β, IL-6, TNF- α and ROS, while blocking the phosphorylation of NF-κB p65 in nucleus by preventing IκB-α degradation and phosphorylation in cytosol.Significance:The present study revealed that VD2 blocked the phosphorylation of NF-κB inflammatory signaling pathway in Aβ25–35 induced activated BV2 microglial cells by suppressing ROS generation and inflammatory cytokines. Our finding suggests that vitamin D2 has therapeutic potential against inflammation and Alzheimer's disease.Graphical abstract:

    loading  Loading Related Articles