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Aspergillusidone G Potentiates the Anti-Inflammatory Effects of Polaprezinc in LPS-Induced BV2 Microglia: A
Fangfang Ban1, Longjian Zhou1,2,3, Zhiyou Yang1,2,3
1Guangdong Provincial Key Laboratory of Aquatic Product Processing and Safety, Guangdong Provincial Engineering Laboratory for Marine Biological Products, Guangdong Provincial Center for Modern Agricultural Scientific Innovation, Shenzhen Institute of Guangdong Ocean University, Zhanjiang Municipal Key Laboratory of Marine Drugs and Nutrition for Brain Health, Research Institute for Marine Drugs and Nutrition, College of Food Science and Technology, Guangdong Ocean University, Zhanjiang 524088, China.
Abstract:
Neuroinflammation is one of the main mechanisms involved in the progression of neurodegenerative diseases (NDs), and microglial activation is the main feature of neuroinflammation. Polaprezinc (Pol), a chelator of L-carnosine and zinc, is widely used as a clinical drug for gastric ulcers. However, its potential effects on NDs remain unexplored. In LPS-induced BV-2 microglia, we found that Pol reduced the generation of NO and ROS and revealed inhibited expression of iNOS, COX-2, and inflammatory factors such as IL-6, TNF-α, and 1L-1β by Pol using qRT-PCR and Western blotting. These effects were found to be associated with the suppression of the NF-κB signaling pathway. Moreover, we evaluated the potential synergistic effects of aspergillusidone G (Asp G) when combined with Pol. Remarkably, co-treatment with low doses of Asp G enhanced the NO inhibition by Pol from approximately 30% to 80% in LPS-induced BV2 microglia, indicating a synergistic anti-inflammatory effect. A bioinformatics analysis suggested that the synergistic mechanism of Asp G and Pol might be attributed to several targets, including NFκB1, NRF2, ABL1, TLR4, and PPARα. These findings highlight the anti-neuroinflammatory properties of Pol and its enhanced efficacy when combined with Asp G, proposing a novel therapeutic strategy for managing neuroinflammation in NDs.
Insights
Polaprezinc reduces neuroinflammation by inhibiting microglial activation. Combined with aspergillusidone G, it shows enhanced anti-inflammatory effects, offering a new strategy for neurodegenerative diseases.
Area of Science:
- Neuroscience
- Pharmacology
Background:
- Neuroinflammation, characterized by microglial activation, drives neurodegenerative diseases (NDs).
- Polaprezinc (Pol), a zinc and L-carnosine chelator, is clinically used for gastric ulcers but its neurological effects are unknown.
Purpose of the Study:
- To investigate the anti-neuroinflammatory effects of Polaprezinc.
- To explore the synergistic potential of aspergillusidone G (Asp G) with Polaprezinc in neuroinflammation.
Main Methods:
- LPS-induced BV-2 microglia model was used.
- Quantitative real-time PCR (qRT-PCR) and Western blotting assessed inflammatory markers.
- NF-κB signaling pathway activity was evaluated.
- Bioinformatics analysis identified potential synergistic targets.
Main Results:
- Polaprezinc significantly reduced nitric oxide (NO) and reactive oxygen species (ROS) generation.
- Pol inhibited inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), and inflammatory cytokines (IL-6, TNF-α, IL-1β).
- Polaprezinc suppressed the NF-κB signaling pathway.
- Co-treatment with low-dose Asp G synergistically enhanced Pol's NO inhibition effect.
- Bioinformatics suggested shared targets including NFκB1, NRF2, ABL1, TLR4, and PPARα for the synergistic action.
Conclusions:
- Polaprezinc exhibits significant anti-neuroinflammatory properties.
- Combining Polaprezinc with aspergillusidone G enhances its efficacy, suggesting a novel therapeutic approach for neuroinflammation in NDs.
