Valproic acid attenuates nitric oxide and interleukin‑1β production in lipopolysaccharide‑stimulated iron‑rich microglia

Mairuae,Nootchanat; Cheepsunthorn,Poonlarp

doi:10.3892/br.2018.1062

Valproic acid attenuates nitric oxide and interleukin‑1β production in lipopolysaccharide‑stimulated iron‑rich microglia

Authors:
- Nootchanat Mairuae
- Poonlarp Cheepsunthorn
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Affiliations: Biomedical Research Unit, Faculty of Medicine, Mahasarakham University, Maha Sarakham 44000, Thailand, Department of Anatomy, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Published online on: February 9, 2018 https://doi.org/10.3892/br.2018.1062
Pages: 359-364

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Abstract

Iron accumulation in activated microglia has been consistently reported in neurodegenerative diseases. Previous results suggest that these cells facilitate neuroinflammation leading to neuronal cell death. Therefore, chemical compounds that alleviate the activation of iron‑rich microglia may result in neuroprotection. In the present study, the effect of valproic acid (VPA) on microglial activation under iron‑rich conditions was investigated. BV‑2 microglial cells were exposed to lipopolysaccharide (LPS; 1 µg/ml) and iron (300 µg/ml) with or without VPA (1.6 mM). The results demonstrated that VPA attenuated the activation of iron‑rich BV2 cells induced by LPS by down‑regulating the mRNA expression of inducible nitric oxide (NO) synthase and interleukin 1β (IL‑1β; P<0.01), to ultimately reduce the production of NO and IL‑1β (P<0.01). These events were accompanied by an attenuation in the nuclear translocation of nuclear factor‑κB p65 subunit (P<0.01). These findings suggest that VPA may be therapeutically useful for attenuating the activation of iron‑rich microglia.

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