Home FOR AUTHORS General Physiology and Biophysics 2019 General Physiology and Biophysics Vol.38, No.2, p.111–122, 2019

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Founded: 1982
ISSN  1338-4325 (online)

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General Physiology and Biophysics Vol.38, No.2, p.111–122, 2019

Title: Catalpol attenuates lipopolysaccharide-induced inflammatory responses in BV2 microglia through inhibiting the TLR4-mediated NF-κB pathway
Author: Yung Hyun Choi

Abstract: Catalpol, an iridoid glucoside mainly found in the root of Rehmannia glutinosa Libosch, is known to possess various pharmacological effects. Here, we investigated its inhibitory potential against inflammatory responses in lipopolysaccharide (LPS)-stimulated BV2 microglia. Our results showed that catalpol significantly suppressed LPS-induced secretion of pro-inflammatory mediators, including nitric oxide (NO) and prostaglandin E2. Consistent with these results, catalpol downregulated LPS-stimulated expression of their regulatory enzymes, such as inducible NO synthase and cyclooxygenase-2. Catalpol also inhibited LPS-induced production and expression of pro-inflammatory cytokines, such as tumor necrosis factor-α and interleukin-1β. Additionally, catalpol suppressed the nuclear factor-kappa B (NF-κB) signaling pathway by disrupting the phosphorylation and degradation of inhibitor of κB-α and blocking the nuclear translocation of NF-κB p65. Moreover, catalpol inhibited LPS-induced expression of toll-like receptor 4 (TLR4) and myeloid differentiation factor 88, which was related to suppression of the binding of LPS with TLR4 on the cell surface. Furthermore, catalpol markedly reduced LPS-induced generation of reactive oxygen species (ROS). Collectively, these results suggest that catalpol can repress LPS-mediated inflammatory action in BV2 microglia through inactivating NF-κB signaling by antagonizing TLR4 and eliminating ROS, indicating that catalpol can have potential benefits by inhibiting the onset and/or treatment of inflammatory diseases.

Keywords: Catalpol, Anti-inflammation, NF-κB, TLR4, ROS
Published online: 25-Mar-2019
Year: 2019, Volume: 38, Issue: 2 Page From: 111, Page To: 122

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