Noscapine Down-Regulates Lps-Induced Neuroinflammation in Bv-2 Microglia Cells Via Modulation of Mapk and Nf-Κb Signaling Pathways

Abstract

Noscapine is widely used to prevent stroke, glioblastoma, and anxiety. The aim of this study was to investigate the anti-neuroinflammatory activity and possible molecular mechanisms of noscapine on lipopolysaccharide (LPS)-induced BV-2 microglia cells. BV2 microglial cells were treated with LPS in the presence and absence of noscapine. In the current study, nitrite, Prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and IL-6 productions, inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) mRNA levels, phosphorylation of NF-kappa B, I kappa B, ERK, JNK, and p38 proteins were measured. Noscapine treatment triggered a significant reduction on nitrite, PGE2, TNF-alpha, IL-6, and IL-1 beta production, iNOS and COX-2 mRNA levels, NF-kappa B, I kappa B, ERK, JNK, and p38 phosphorylation in LPS-induced BV-2 microglia cells. The results of this study demonstrate the efficiency of noscapine as a potent anti-inflammatory agent. It can be suggested that noscapine has suppressed LPS-induced neuroinflammation in BV-2 microglia cells in the current study, and thus noscapine can be utilized as an efficient anti-neuroinflammatory agent.