Sauchinone suppresses lipopolysaccharide-induced inflammatory responses through Akt signaling in BV2 cells

Sec-O-glucosylhamaudol suppressed inflammatory reaction induced by LPS in RAW264.7 cells through inhibition of NF-κB and MAPKs signaling

“…NF-κB was released from the cytoplasmic NF-κB-IκB-α complex, and free NF-κB was translocated into the nucleus, in which it was bound to NF-κB sites in the promoter region of genes for some pro-inflammatory cytokines or inflammatory mediators [4,16]. Several previous studies reported that some natural compounds such as schisantherin A, sauchinone and arctigenin exerted their anti-inflammatory impact by blocking MAPK and NF-κB signaling pathways [19][20][21]. To investigate whether SOG can inhibit the expression of TNF-α and IL-6 in LPS-stimulated RAW264.7 cells via blocking NF-κB signaling pathway, the effects of SOG on the degradation of IκB-α degradation and NF-κB p65 subunit phosphorylation were thus measured.…”

Attenuation of inflammatory-mediated neurotoxicity by Saururus chinensis extract in LPS-induced BV-2 microglia cells via regulation of NF-κB signaling and anti-oxidant properties

“…SC contains several compounds such as saucerneol D/F, sauchinone, manassantin A and B dineolignans and quercetin (QCT) flavonol glycosides [ 24 – 28 ]. These compounds were well reported to possess various biological activities including anti-inflammatory activities [ 11 , 26 , 49 – 52 ]. In our present study HPLC fingerprint analysis showed that SC extract contained QCT as one of the major compounds compared with reference standard.…”

SMEAF attenuates the production of pro-inflammatory mediators through the inactivation of Akt-dependent NF-κB, p38 and ERK1/2 pathways in LPS-stimulated BV-2 microglial cells

“…Microglia are activated by a broad spectrum of stimuli such as lipopolysaccharide (LPS), interferon-γ (IFN-γ), or β-amyloid (Choi & Park, 2012;Glass, Saijo, Winner, Marchetto, & Gage, 2010;Jang, Yang, Han, Choi, & Hwang, 2012). The activation of microglia by these stimuli produces various pro-inflammatory factors that simultaneously affect the surrounding neurons and cause neuronal damage Schlegelmilch, Henke, & Peri, 2011).…”

“…The activated microglia will undergo organized responses by the activation of NF-κB as well as several intracellular inflammation signalling pathways including Akt, p38 MAPK and ERK1/2 Zeng, Wang, Dong, Jiang, & Tu, 2014). Increasing reports showed that the activation of NF-κB and these intracellular signalling pathways have significant roles in the transcription of inflammation-associated genes followed by production and secretion of pro-inflammatory or neurotoxic factors such as tumor necrosis factor (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), nitric oxide (NO), prostaglandin E2 (PGE2), and reactive oxygen species (ROS) (Candiracci et al, 2012;Choi & Park, 2012;Jang et al, 2012;Lai et al, 2011;Zeng et al, 2014). Under normal condition, the microglia produce and secrete a sufficient amount of pro-inflammatory factors primarily for defence purposes.…”

“…Under normal condition, the microglia produce and secrete a sufficient amount of pro-inflammatory factors primarily for defence purposes. However, the exacerbated activation of microglia leads to overproduction of the pro-inflammatory factors that eventually promotes neuronal damage and leads to various neurodegenerative diseases including Alzheimer's diseases (AD), Parkinson's diseases (PD), amyotrophic lateral sclerosis, cerebral ischaemia and MAP-induced neurotoxicity (Arranz et al, 2015;Choi & Park, 2012;Jang et al, 2012;Stansley, Post, & Hensley, 2012). Thus, modulation of microglia activation is an important therapeutic target in the treatment of various neurodegenerative diseases (Choi & Park, 2012;de Oliveira et al, 2012;Kim et al, 2012).…”