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Sodium P-aminosalicylic Acid Attenuates Manganese-Induced Neuroinflammation in BV2 Microglia by Modulating NF-κB
Junyan Li1,2, Yue Deng1,2, Dongjie Peng1,2
1Department of Toxicology, School of Public Health, Guangxi Medical University, Shuang-yong Road No.22, Nanning, 530021, Guangxi, China.
Abstract:
Exposure to high levels of manganese (Mn) leads to brain Mn accumulation, and a disease referred to as manganism. Activation of microglia plays an important role in Mn-induced neuroinflammation. Sodium p-aminosalicylic acid (PAS-Na) is a non-steroidal anti-inflammatory drug that inhibits Mn-induced neuroinflammation. The aim of the current study was to explore the role of NF-κB in the protective mechanism of PAS-Na on Mn-induced neuroinflammation in BV2 microglial experimental model. We treated BV2 microglia with 200 μM Mn for 24 h followed by 48 h treatment with graded concentrations of PAS-Na, using an NF-kB inhibitor, JSH-23, as a positive control. MTT results established that 200 and 400 μM PAS-Na treatment increased the Mn-induced cell viability reduction. NF-κB (P65) mRNA expression and the phosphorylation of p65 were increased in Mn-treated BV2 cell, and suppressed by PAS-Na, analogous to the effect of JSH-23 pretreatment. Furthermore, PAS-Na significantly reduced the contents of the inflammatory cytokine TNF-α and IL-1β, both of which were increased by Mn treatment. The current results show that PAS-Na attenuated Mn-induced inflammation by abrogating the activation of the NF-κB signaling pathways and reduced the release of pro-inflammatory cytokines.
Insights
Sodium p-aminosalicylic acid (PAS-Na) protects against manganese-induced neuroinflammation by inhibiting the NF-κB pathway. This anti-inflammatory drug reduces microglial activation and pro-inflammatory cytokine release, offering a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Toxicology
- Pharmacology
Background:
- High manganese (Mn) exposure causes brain accumulation and manganism.
- Microglial activation is central to Mn-induced neuroinflammation.
- Sodium p-aminosalicylic acid (PAS-Na) is an anti-inflammatory drug with potential to mitigate Mn toxicity.
Purpose of the Study:
- To investigate the protective role of PAS-Na against Mn-induced neuroinflammation in BV2 microglia.
- To elucidate the involvement of the NF-κB signaling pathway in PAS-Na's protective mechanism.
Main Methods:
- BV2 microglia were exposed to manganese (Mn).
- Cells were subsequently treated with varying concentrations of Sodium p-aminosalicylic acid (PAS-Na) or NF-κB inhibitor JSH-23.
- Cell viability (MTT assay), NF-κB (P65) mRNA expression, p65 phosphorylation, and pro-inflammatory cytokines (TNF-α, IL-1β) were analyzed.
Main Results:
- PAS-Na (200 and 400 μM) improved cell viability reduced by Mn exposure.
- Mn exposure increased NF-κB (P65) mRNA and p65 phosphorylation, which PAS-Na and JSH-23 suppressed.
- PAS-Na significantly decreased Mn-induced increases in TNF-α and IL-1β.
Conclusions:
- PAS-Na demonstrates neuroprotective effects against manganese toxicity in microglia.
- The mechanism involves the suppression of NF-κB signaling pathway activation.
- PAS-Na reduces the release of key pro-inflammatory cytokines, suggesting therapeutic potential for manganism.
