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Published on: January 30, 2014
Vitamin D2 suppresses amyloid-β 25-35 induced microglial activation in BV2 cells by blocking the NF-κB inflammatory
Suchismita Raha1, Ho Jeong Lee1, Silvia Yumnam1
1Research Institute of Life Science and College of Veterinary Medicine (BK21 plus project), Gyeongsang National University, Gazwa, Jinju 660-701, Republic of Korea.
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 24h 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.
Insights
Vitamin D2 (VD2) reduces inflammation in Alzheimer's disease models by inhibiting microglial activation. This study shows VD2 suppresses inflammatory responses and oxidative stress, suggesting its therapeutic potential for neurodegenerative diseases.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Vitamin D deficiency is linked to inflammation and neurodegenerative diseases like Alzheimer's disease (AD).
- Microglial activation is central to AD pathogenesis, driving inflammation and neuronal injury.
- Vitamin D2 (VD2) possesses anti-inflammatory properties that warrant further investigation in AD contexts.
Purpose of the Study:
- To investigate the inhibitory effects of vitamin D2 (VD2) on the inflammatory activities of BV2 microglial cells.
- To explore VD2's potential as a therapeutic agent against inflammation and Alzheimer's disease.
Main Methods:
- Cellular compatibility of VD2 and amyloid-beta (Aβ25-35) was assessed using CCK-8 assays.
- Western blotting was employed to measure inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and nuclear factor-kappa B (NF-κB) signaling.
- Enzyme-linked immunosorbent assay (ELISA) quantified pro-inflammatory cytokines, and fluorescence intensity detected reactive oxygen species (ROS) generation.
Main Results:
- VD2 pre-treatment significantly reduced Aβ25-35-induced BV2 cell stimulation.
- VD2 inhibited iNOS and COX-2 protein expression, attenuated pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), and reduced ROS generation.
- VD2 blocked NF-κB p65 phosphorylation by preventing IκB-α degradation in the cytosol.
Conclusions:
- Vitamin D2 effectively suppresses the NF-κB inflammatory signaling pathway in Aβ25-35-induced activated BV2 microglial cells.
- VD2 mitigates inflammation by reducing ROS generation and pro-inflammatory cytokine release.
- These findings highlight vitamin D2's therapeutic potential for managing inflammation and Alzheimer's disease.
