Magnolol inhibits Streptococcus suis-induced inflammation and ROS formation via TLR2/MAPK/NF-κB signaling in RAW264.7 cells.

  title={Magnolol inhibits Streptococcus suis-induced inflammation and ROS formation via TLR2/MAPK/NF-$\kappa$B signaling in RAW264.7 cells.},
  author={Lin Zhang and Jinli Wang and W Xu and Yingxian Sun and Ju-yeon You and H. Lu and Y T Song and J Wei and Lijing Li},
  journal={Polish journal of veterinary sciences},
  volume={21 1},
  • L. Zhang, J. Wang, +6 authors L. Li
  • Published 2018
  • Medicine, Biology
  • Polish journal of veterinary sciences
Our previous studies have shown that Magnolol (Mag) improves the symptoms and decreases the levels of cytokines during infection induced by Streptococcus suis (S. suis) in mice. Although some reports show that Mag inhibits lipopolysaccharide-induced inflammatory responses via downregulating mitogen-activated protein kinases (MAPK) and nuclear factor-κB (NF-κB) signaling pathways, the molecular mechanisms underlying Mag-mediated inhibition of S. suis-induced inflammatory responses are poorly… Expand
Baicalin inhibits Salmonella typhimurium‐induced inflammation and mediates autophagy through TLR4/MAPK/NF‐κB signalling pathway
The findings indicated that Baicalin exerts anti‐inflammatory and cell‐protective effects, and it mediates autophagy by down‐regulating the activity of TLR4 infected by S typhimurium. Expand
Sophorasubprosrate polysaccharide suppress the inflammatory reaction of RAW264.7 cells infected with PCV2 via regulation NF-κB/MAPKs/c-Jun signal pathway and histone acetylation modification.
The findings indicated that the molecular mechanism of how traditional Chinese medicine polysaccharide regulates inflammatory signal pathways and inflammatory factors by regulating histone acetylation may be regulated by SSP. Expand
In vitro characterization of granulocyte-colony stimulating factor (G-CSF) production by dendritic cells and macrophages during Streptococcus suis infection.
It is demonstrated for the first time that S. suis induces G-CSF production in vivo and DCs and macrophages are key cellular sources of this cytokine mediator, mainly via the binding of lipoproteins to TLR2. Expand
Simvastatin Improves Cardiac Hypertrophy in Diabetic Rats by Attenuation of Oxidative Stress and Inflammation Induced by Calpain-1-Mediated Activation of Nuclear Factor-κB (NF-κB)
  • Qianqian Han, Q. Liu, +4 authors Yingjie Zhang
  • Medicine, Chemistry
  • Medical science monitor : international medical journal of experimental and clinical research
  • 2019
Simvastatin improved the cardiac hypertrophy of diabetic rats, as demonstrated by decreases in the ratios of left ventricular weight/body weight (LVW/ BW) and heart weight/ body weight (HW/BW) and by the downregulation of mRNA expression of BNP and ANP in the heart tissue. Expand
Magnolol alleviates Alzheimer's disease-like pathology in transgenic C. elegans by promoting microglia phagocytosis and the degradation of beta-amyloid through activation of PPAR-γ.
MG dose-dependently reduces Aβ deposition, toxicity and memory impairment caused by Aβ in transgenic C. elegans and the underlying mechanism is the reduction of inflammation and promotion of phagocytosis and degradation of Aβ, which is dependent on PPAR-γ. Expand
Antinociceptive Effect of Magnolol in a Neuropathic Pain Model of Mouse
The findings indicate that Mag has antinociceptive effect on neuropathic pain, probably mediated through P2Y12 receptors and p38 MAPK mediated pathways, and with its relatively safe profile, Mag may be a potential therapeutic agent for neuropathicPain. Expand
Pharmacology, Toxicity, Bioavailability, and Formulation of Magnolol: An Update
This review provides an actualization of already known anti-inflammatory, cardiovascular protection, antiangiogenesis, antidiabetes, hypoglycemic, antioxidation, neuroprotection, gastrointestinal protection, and antibacterial activities of Magnoliae officinalis cortex. Expand
Potential of phytomedicine in the treatment of inflammatory bowel disease
  • Jie Tang, Dong Xu, +5 authors Yuan-Lu Cui
  • Medicine
  • 2021
This paper summarizes the experimental research on IBD from the perspective of phytomedicine according to the structural classification of phytonutrient and provides a reference for the further development of new IBD therapies. Expand


Polydatin ameliorates Staphylococcus aureus-induced mastitis in mice via inhibiting TLR2-mediated activation of the p38 MAPK/NF-κB pathway
PD does not exhibit antibacterial activity against S aureus, its therapeutic effects in mouse S a Aureus-induced mastitis depend on its ability to down-regulate pro-inflammatory cytokine levels via inhibiting TLR2-mediated activation of the p38 MAPK/NF-κB signaling pathway. Expand
Magnolol potently suppressed lipopolysaccharide-induced iNOS and COX-2 expression via downregulating MAPK and NF-κB signaling pathways
Abstract Magnolol is a hydroxylated biphenyl compound from the bark of Magnolia officinalis that has been reported to have various biological properties including anti-inflammation. However, theExpand
Activation of Nrf2/HO-1signaling pathway involves the anti-inflammatory activity of magnolol in Porphyromonas gingivalis lipopolysaccharide-stimulated mouse RAW 264.7 macrophages.
A novel mechanism by which magnolol inhibits P. gingivalis LPS-induced inflammation in macrophages is at least partly mediated by HO-1 activation, and thereby promoting its clinical use in periodontitis is provided. Expand
Magnolol inhibits lipopolysaccharide-induced inflammatory response by interfering with TLR4 mediated NF-κB and MAPKs signaling pathways.
The results suggest that magnolol exerts an anti-inflammatory property by down-regulated the expression of TLR4 up-regulated by LPS, thereby attenuatingTLR4 mediated the activation of NF-κB and MAPK signaling and the release of pro-inflammatory cytokines. Expand
Magnolol Inhibits the Inflammatory Response in Mouse Mammary Epithelial Cells and a Mouse Mastitis Model
Investigating the protective effects of magnolol on inflammation in lipopolysaccharide (LPS)-induced mastitis mouse model in vivo and the mechanism of this protective effects in LPS-stimulated mouse mammary epithelial cells (MMECs) in vitro demonstrated thatMagnolol may be a therapeutic agent against mastitis. Expand
Proinflammatory cytokine and chemokine modulation by Streptococcus suis in a whole-blood culture system.
The presence of specific antibodies suppressed bacterial growth resulting in significantly reduced levels of cytokine production, providing first evidence of S. suis-induction of pro-inflammatory swine cytokines. Expand
Herbal remedy magnolol suppresses IL‐6‐induced STAT3 activation and gene expression in endothelial cells
The results indicate that Mag inhibits IL‐6‐induced STAT3 activation and subsequently results in the suppression of downstream target gene expression in ECs, providing a therapeutic basis for the development of Mag as an anti‐inflammatory agent for vascular disorders including atherosclerosis. Expand
Genistein Inhibits Osteoclastic Differentiation of RAW 264.7 Cells via Regulation of ROS Production and Scavenging
The results provide that the inhibitory effects of genistein on RANKL-stimulated osteoclast differentiation is likely to be attributed to the control of ROS generation through suppressing the translation and activation of Nox1 and the disruption of the mitochondrial electron transport chain system, as well as ROS scavenging through the Nrf2-mediated induction of phase II antioxidant enzymes, such as SOD1 and HO-1. Expand
Ginsenosides compound K and Rh(2) inhibit tumor necrosis factor-alpha-induced activation of the NF-kappaB and JNK pathways in human astroglial cells.
Results collectively indicate that ginsenoside metabolites C-K and Rh(2) exert anti-inflammatory effects by the inhibition of both NF-kappaB and JNK pathways in a cell-specific manner. Expand
Sodium Octanoate Modulates the Innate Immune Response of Bovine Mammary Epithelial Cells through the TLR2/P38/JNK/ERK1/2 Pathway: Implications during Staphylococcus aureus Internalization
1 mM NaO activates bMECs via the TLR2 signaling pathways (p38, JNK, and ERK1/2), which improves IIR before S. aureus invasion and might exert anti-inflammatory effects after bacterial internalization. Expand