Qing Hua Chang Yin attenuates lipopolysaccharide-induced inflammatory response in human intestinal cells by inhibiting NF-κB activation

Abstract

Ulcerative colitis (UC) is a major form of inflammatory bowel disease (IBD), which is tightly regulated by the nuclear factor κB (NF-κB) pathway. Thus, the suppression of NF-κB signaling may provide a promising strategy for the treatment of UC. Qing Hua Chang Yin (QHCY) is a traditional Chinese formulation, which has been used for a number of years to clinically treat UC. However, little is known with regard to its anti-inflammatory properties. In the present study, lipopolysaccharide (LPS)-stimulated Caco-2 cells were used as an in vitro inflammatory model of the human intestinal epithelium to evaluate the anti-inflammatory effects of QHCY and its underlying molecular mechanisms. We observed that QHCY inhibited the inflammatory response in intestinal epithelial cells as it significantly and concentration-dependently reduced the LPS-induced secretion of pro-inflammatory TNF-α and IL-8 in Caco-2 cells. Furthermore, QHCY treatment inhibited the phosphorylation of IκB and the nuclear translocation of NF-κB in Caco-2 cells in a concentration-dependent manner, indicating that QHCY suppressed the activation of the NF-κB signaling pathway. Collectively, our results suggest that the inhibition of NF-κB-mediated inflammation may constitute a potential mechanism by which QHCY treats UC.

Aspirin attenuates angiotensin II-induced inflammation in bone marrow mesenchymal stem cells via the inhibition of ERK1/2 and NF-κB activation

“…In addition, we also observed that aspirin markedly inhibited the Ang II-induced activation of NF-κB. NF-κB is another important factor involved in inflammation (19). Previous studies demonstrated that aspirin inhibits the activation of NF-κB pathway in certain chronic inflammatory conditions, protecting organs and tissues from inflammation and damage (20)(21)(22).…”

Intraperitoneal administration of butyrate prevents the severity of acetic acid colitis in rats

“…The production of these pro-inflammatory cytokines is mediated mainly by transcriptional activation of nuclear factor κB (NF-κB) and mitogen activated protein kinase (MAPK) pathways (Malago et al, 2002;Ke et al, 2013). Several therapeutic interventions such as butyrate enemas modulate the activation of these pathways and suppress the production of pro-inflammatory cytokines to protect the colon against inflammatory injury (Venkatraman et al, 2003;Malago et al, 2005;Ke et al, 2013).…”

“…Continual activation of the immune system to produce proinflammatory chemokines like interleukin (IL)-8 and their subsequent attraction of inflammatory cells that infiltrate the colon mucosa are cascade events that cause the chronic inflammation and ulceration of the colonic epithelium (Malago and Nondoli, 2008;Ke et al, 2013;Liu et al, 2013). The production of these pro-inflammatory cytokines is mediated mainly by transcriptional activation of nuclear factor κB (NF-κB) and mitogen activated protein kinase (MAPK) pathways (Malago et al, 2002;Ke et al, 2013). Several therapeutic interventions such as butyrate enemas modulate the activation of these pathways and suppress the production of pro-inflammatory cytokines to protect the colon against inflammatory injury (Venkatraman et al, 2003;Malago et al, 2005;Ke et al, 2013).…”

Gene expression profiles in the intestine of lipopolysaccharide-challenged piglets

“…Similarly, LPS administration increased the mRNA levels for IL-1β, chemokines (CXCL9, CXCL10, and CXCL11), TLR4, and NF-κB in the jejunum (Table 4). As a main component of the outer membrane of Gram negative bacteria, LPS directly activates the host toll-like receptor 4 (TLR4), which subsequently transduces immune-related signals to the nucleus via transcription factors, including NF-κB (73), leading to the transcription of various proinflammatory cytokines (74). Therefore, the TLR4-NF-κB signaling pathway may be the main mechanism involved in the immune response to LPS in porcine intestine.…”