Magnolol attenuates sepsis-induced gastrointestinal dysmotility in rats by modulating inflammatory mediators

Abstract

AIM:To investigate the protective effects of magnolol on sepsis-induced inflammation and intestinal dysmotility. METHODS: Sepsis was induced by a single intraperitoneal injection of lipopolysaccharide (LPS). Male Wistar ratswere randomly assigned to one of three treatment groups: magnolol prior to LPS injection (LPS/Mag group); vehicle prior to LPS injection (LPS/Veh group); vehicle prior to injection of saline (Control/Veh). Intestinal transit and circular muscle mechanical activity were assessed 12 h after LPS injection. Tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), monocyte chemoattractant protein-1 (MCP-1) and inducible nitric oxide synthase (iNOS) mRNA in rat ileum were studied by RT-PCR 2 h after LPS injection. Nuclear factor-κB (NF-κB) activity in the intestine was also investigated at this time using electrophoretic mobility shift assay. In addition, antioxidant activity was determined by measuring malondialdehyde (MDA) concentration and superoxide dismutase (SOD) activity in the intestine 2 h after LPS injection. RESULTS:Magnolol significantly increased intestinal transit and circular muscle mechanical activity in LPStreated animals. TNF-α, MCP-1 and iNOS mRNA expression in the small intestine were significantly reduced after magnolol treatment in LPS-induced septic animals, compared with untreated septic animals. Additionally, magnolol significantly increased IL-10 mRNA expression in septic rat ileum. Magnolol also significantly suppressed NF-κB activity in septic rat intestine. In addition, magnolol significantly decreased MDA concentration and increased SOD activity in rat ileum. CONCLUSION: Magnolol prevents sepsis-inducedsuppression of intestinal motility in rats. The potential mechanism of this benefit of magnolol appears to be modulation of self-amplified inflammatory events and block of oxidative stress in the intestine.

Magnolol inhibits lipopolysaccharide-induced inflammatory response by interfering with TLR4 mediated NF-κB and MAPKs signaling pathways

“…Magnolol, the major biphenyl compound ingredient of gardenia herbs, has emerged as a novel multifunctional tissue-protective agent with anti-edematous and anti-inflammatory effects (Yang et al, 2008). The pro-inflammatory cytokines play an important role in inflammatory diseases.…”

Magnolol Reduces Renal Ischemia and Reperfusion Injury via Inhibition of Apoptosis

“…Yunhe et al (2012) demonstrated that magnolol attenuates the severity of lipopolysaccharide-induced lung injury and down-regulates the levels of TNF-α, IL-1β and IL-6 in mice. Yang et al (2008) reported that magnolol reduces gastrointestinal dysmotility in lipopolysaccharide-induced septic rats. In that study, the TNF-α mRNA expression in the small intestine was significantly reduced after magnolol treatment, while IL-10 mRNA expression was significantly increased in the ileum of magnolol-treated septic rats.…”

Magnolol potently suppressed lipopolysaccharide-induced iNOS and COX-2 expression via downregulating MAPK and NF-κB signaling pathways

“…Furthermore, several studies also demonstrated that magnolol has a board spectrum of anti-inflammatory effect. Magnolol was found to suppress the expression of the inducible nitric oxide synthase (iNOS) in macrophages (Matsuda et al, 2001), to inhibit inflammatory cytokines production in THP-1 cells and to attenuate septic shock in rats induced by surgical and endotoxin (Tsai et al, 2010;Yang, Zhang, Sun, Wang, & Ren, 2008). In addition, a recent study also showed that treatment with magnolol strongly inhibited TPA-induced skin inflammation and againsts DMBA/TPA-induced skin tumorigenesis in mice (Kuo et al, 2010).…”