scholarly journals Zerumbone Suppresses Enterotoxigenic Bacteroides fragilis Infection-Induced Colonic Inflammation through Inhibition of NF-κΒ

2019 ◽  
Vol 20 (18) ◽  
pp. 4560 ◽  
Author(s):  
Soonjae Hwang ◽  
Minjeong Jo ◽  
Ju Eun Hong ◽  
Chan Oh Park ◽  
Chang Gun Lee ◽  
...  
Keyword(s):  
Bacteroides Fragilis ◽  
Serum Levels ◽  
Colonic Inflammation ◽  
Colon Cells ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide ◽  
Inflammatory Effect ◽  
E Cadherin

Enterotoxigenic Bacteroides fragilis (ETBF) is human intestinal commensal bacterium and a potent initiator of colitis through secretion of the metalloprotease Bacteroides fragilis toxin (BFT). BFT induces cleavage of E-cadherin in colon cells, which subsequently leads to NF-κB activation. Zerumbone is a key component of the Zingiber zerumbet (L.) Smith plant and can exhibit anti-bacterial and anti-inflammatory effects. However, whether zerumbone has anti-inflammatory effects in ETBF-induced colitis remains unknown. The aim of this study was to determine the anti-inflammatory effect of orally administered zerumbone in a murine model of ETBF infection. Wild-type C57BL/6 mice were infected with ETBF and orally administered zerumbone (30 or 60 mg/kg) once a day for 7 days. Treatment of ETBF-infected mice with zerumbone prevented weight loss and splenomegaly and reduced colonic inflammation with decreased macrophage infiltration. Zerumbone treatment significantly decreased expression of IL-17A, TNF-α, KC, and inducible nitric oxide synthase (iNOS) in colonic tissues of ETBF-infected mice. In addition, serum levels of KC and nitrite was also diminished. Zerumbone-treated ETBF-infected mice also showed decreased NF-κB signaling in the colon. HT29/C1 colonic epithelial cells treated with zerumbone suppressed BFT-induced NF-κB signaling and IL-8 secretion. However, BFT-mediated E-cadherin cleavage was unaffected. Furthermore, zerumbone did not affect ETBF colonization in mice. In conclusion, zerumbone decreased ETBF-induced colitis through inhibition of NF-κB signaling.

scholarly journals Dipterocarpus tuberculatus Roxb. Ethanol Extract Has Anti-Inflammatory and Hepatoprotective Effects In Vitro and In Vivo by Targeting the IRAK1/AP-1 Pathway

Molecules ◽  
2021 ◽  
Vol 26 (9) ◽  
pp. 2529
Author(s):  
Haeyeop Kim ◽  
Woo Seok Yang ◽  
Khin Myo Htwe ◽  
Mi-Nam Lee ◽  
Young-Dong Kim ◽  
...  
Keyword(s):  
Ethanol Extract ◽  
Serum Levels ◽  
Hepatoprotective Activity ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Related Proteins ◽  
Pro Inflammatory Cytokines ◽  
Inflammatory Effect

Dipterocarpus tuberculatus Roxb. has been used traditionally as a remedy for many diseases, especially inflammation. Therefore, we analyzed and explored the mechanism of the anti-inflammatory effect of a Dipterocarpus tuberculatus Roxb. ethanol extract (Dt-EE). Dt-EE clearly and dose-dependently inhibited the expression of pro-inflammatory cytokines such as IL-6, TNF-α, and IL-1β in lipopolysaccharide (LPS)-treated RAW264.7 cells. Also, Dt-EE suppressed the activation of the MyD88/TRIF-mediated AP-1 pathway and the AP-1 pathway related proteins JNK2, MKK4/7, and TAK1, which occurred as a result of inhibiting the kinase activity of IRAK1 and IRAK4, the most upstream factors of the AP-1 pathway. Finally, Dt-EE displayed hepatoprotective activity in a mouse model of hepatitis induced with LPS/D-galactosamine (D-GalN) through decreasing the serum levels of alanine aminotransferase and suppressing the activation of JNK and IRAK1. Therefore, our results strongly suggest that Dt-EE could be a candidate anti-inflammatory herbal medicine with IRAK1/AP-1 inhibitory and hepatoprotective properties.

scholarly journals Dried Ginger (Zingiber officinalis) Inhibits Inflammation in a Lipopolysaccharide-Induced Mouse Model

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
You Yeon Choi ◽  
Mi Hye Kim ◽  
Jongki Hong ◽  
Sung-Hoon Kim ◽  
Woong Mo Yang
Keyword(s):  
Water Extract ◽  
Clinical Settings ◽  
Protein Factor ◽  
Therapeutic Benefits ◽  
History Of ◽  
Human Use ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide ◽  
Inflammatory Effect

Objectives. Ginger rhizomes have a long history of human use, especially with regards to their anti-inflammatory properties. However, the mechanisms by which ginger acts on lipopolysaccharide-(LPS-)induced inflammation have not yet been identified. We investigated the anti-inflammatory effects of driedZingiber officinalis(DZO) on LPS-induced hepatic injury.Methods. ICR mice were given a DZO water extract (100, 1000 mg/kg) orally for three consecutive days. On the third day, they were administered by LPS intraperitoneally. To investigate the anti-inflammatory effects of DZO, histological, cytokine expression, and protein factor analyses were performed.Results. Oral administration of DZO significantly reduced pathological changes in the liver and proinflammatory cytokines including interferon-(IFN-)γand interleukin-(IL-)6 in the serum. In addition, DZO inhibited LPS-induced NF-κB activation by preventing degradation of the IκB-α, as well as the phosphorylation of ERK1/2, SAPK/JNK, and p38 MAPKs. These were associated with a decrease in the expression of inducible nitric oxide synthase (iNOS) and cyclooxyenase-2 (COX-2).Conclusions. Our data provide evidence for the hepatoprotective mechanisms of DZO as an anti-inflammatory effect. Furthermore, use of DZO to treat could provide therapeutic benefits in clinical settings.

scholarly journals Anti-Inflammatory Effect of 1,3,5,7-Tetrahydroxy-8-isoprenylxanthone Isolated from Twigs ofGarcinia esculentaon Stimulated Macrophage

2015 ◽  
Vol 2015 ◽  
pp. 1-11 ◽  
Author(s):  
Dan-Dan Zhang ◽  
Hong Zhang ◽  
Yuan-zhi Lao ◽  
Rong Wu ◽  
Jin-wen Xu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Diseases ◽  
Inflammatory Activity ◽  
Drug Candidates ◽  
P38mapk Signaling ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide ◽  
Inflammatory Effect

GarciniaLinn. plants having rich natural xanthones and benzophenones with anti-inflammatory activity attracted a great deal of attention to discover and develop them as potential drug candidates. Through screening targeting nitric oxide accumulation in stimulated macrophage, we found that 1,3,5,7-tetrahydroxy-8-isoprenylxanthone (TIE) had potential anti-inflammatory effect. To understand how TIE elicits its anti-inflammatory activity, we uncovered that it significantly inhibits the production of nitric oxide (NO) and prostaglandin E2 (PGE2) in LPS/IFNγ-stimulated RAW264.7 cells. In further study, we showed that TIE reduced the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), two key molecules responsible for the production of NO and PGE2 during inflammation progress. Additionally, TIE also suppressed the expression of inflammatory cytokines IL-6, IL-12, and TNF-α. TIE-led suppression in iNOS, COX-2, and cytokines production were probably the consequence of TIE’s capability to block ERK and p38MAPK signaling pathway. Moreover, TIE blocked activation of nuclear factor-kappa B (NF-κB) as well as NF-κB regulation of miR155 expression. Our study suggests that TIE may represent as a potential therapeutic agent for the treatment of inflammatory diseases.

scholarly journals Bioactive Diterpenes, Norditerpenes, and Sesquiterpenes from a Formosan Soft Coral Cespitularia sp.

2021 ◽  
Vol 14 (12) ◽  
pp. 1252
Author(s):  
You-Cheng Lin ◽  
Chi-Chien Lin ◽  
Yi-Chia Chu ◽  
Chung-Wei Fu ◽  
Jyh-Horng Sheu
Keyword(s):  
Nitric Oxide ◽  
Soft Coral ◽  
2D Nmr ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Chemical investigation of the soft coral Cespitularia sp. led to the discovery of twelve new verticillane-type diterpenes and norditerpenes: cespitulins H–O (1–8), one cyclic diterpenoidal amide cespitulactam L (9), norditerpenes cespitulin P (10), cespitulins Q and R (11 and 12), four new sesquiterpenes: cespilins A–C (13–15) and cespitulolide (16), along with twelve known metabolites. The structures of these metabolites were established by extensive spectroscopic analyses, including 2D NMR experiments. Anti-inflammatory effects of the isolated compounds were studied by evaluating the suppression of pro-inflammatory protein tumor necrosis factor-α (TNF-α) and nitric oxide (NO) overproduction, and the inhibition of the gene expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in lipopolysaccharide-induced dendritic cells. A number of these metabolites were found to exhibit promising anti-inflammatory activities.

scholarly journals Baicalin Administered Orally After Ischemia/Reperfusion Alleviated Brain Injury in Mice by Inhibiting Inflammation and Edema

2019 ◽  
Vol 14 (5) ◽  
pp. 1934578X1984303
Author(s):  
Byoungho Lee ◽  
Chiyeon Lim ◽  
Sehyun Lim ◽  
Suin Cho
Keyword(s):  
Lipid Peroxidation ◽  
Brain Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Pharmacological Activities ◽  
Once Daily ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Water Contents ◽  
Inflammatory Effect

Baicalin is a natural product isolated from Scutellaria genus and has been reported to have many different pharmacological activities, which include anti-viral, anti-inflammatory, and anti-allergic effects. We investigated the effects of baicalin administered after I/R-induced brain injury in a mouse model. I/R-induced brain injury was induced by MCAO for 2 h. Baicalin was orally administered to mice once daily for 2 consecutive days after 2 h of reperfusion. Single daily oral administrations of baicalin at 10, 30, or 100 mg/kg/day for 2 consecutively days after I/R significantly reduced infarct volumes, edema indices, and water contents in mouse brains, serum levels of AQP-4. IL-1β, TNF-α, and ROS, and lipid peroxidation levels in brain ipsilateral hemispheres were suppressed by baicalin. This result is believed to be due to the anti-inflammatory effect of baicalin and its downregulation of AQP-4 protein expression in affected brain tissues after I/R-induced brain injury in mice.

scholarly journals Urocortins and CRF receptor type 2 variants in the male rat colon: gene expression and regulation by endotoxin and anti-inflammatory effect

2016 ◽  
Vol 310 (6) ◽  
pp. G387-G398 ◽  
Author(s):  
Pu-Qing Yuan ◽  
S. Vincent Wu ◽  
Charalabos Pothoulakis ◽  
Yvette Taché
Keyword(s):  
Colonic Mucosa ◽  
Mrna Level ◽  
Male Rat ◽  
Rat Colon ◽  
Tnf Α ◽  
Oxide Synthase ◽  
The Brain ◽  
Inducible Nitric Oxide ◽  
Inflammatory Effect

Urocortins (Ucns) 1, 2, and 3 and corticotropin-releasing factor receptor 2 (CRF2) mRNA are prominently expressed in various layers of the upper gut. We tested whether Ucns and CRF2 variants are also expressed in the different layers of the rat colon, regulated by LPS (100 μg/kg ip) and play a modulatory role in the colonic immune response to LPS. Transcripts of Ucns and CRF2b, the most common isoform in the periphery, were detected in all laser microdissected layers, including myenteric neurons. LPS increased the mRNA level of Ucn 1, Ucn 2, and Ucn 3 and decreased that of CRF2b in both the colonic mucosa and submucosa + muscle (S+M) layers at 2, 6, and 9 h after injection with a return to basal at 24 h. In addition, CRF2a, another variant more prominent in the brain, and a novel truncated splice variant CRF2a-3 mRNA were detected in all segments of the large intestine. LPS reciprocally regulated the colonic expression of these CRF2 variants by decreasing both CRF2a and CRF2b, while increasing CRF2a-3 in the mucosa and S+M. The CRF2 antagonist astressin2-B further enhanced LPS-induced increase of mRNA level of interleukin (IL)-1β, TNF-α, and inducible nitric oxide synthase in S+M layers and IL-1β in the mucosa and evoked TNF-α expression in the mucosa. These data indicate that Ucns/CRF2 variants are widely expressed in all colonic layers and reciprocally regulated by LPS. CRF2 signaling dampens the CD14/TLR4-mediated acute inflammatory response to Gram-negative bacteria in the colon.

GH-releasing peptide-2 administration prevents liver inflammatory response in endotoxemia

2008 ◽  
Vol 294 (1) ◽  
pp. E131-E141 ◽  
Author(s):  
Miriam Granado ◽  
Ana Isabel Martín ◽  
María López-Menduiña ◽  
Asunción López-Calderón ◽  
M. Angeles Villanúa
Keyword(s):  
Receptor Agonist ◽  
Serum Levels ◽  
Ghrelin Receptor ◽  
Nonparenchymal Cells ◽  
Tnf Α ◽  
Igf I ◽  
Ghrelin Receptor Agonist ◽  
Anti Inflammatory ◽  
Inflammatory Effect

It has been reported that growth hormone (GH)-releasing peptide-2 (GHRP-2), a ghrelin receptor agonist, has an anti-inflammatory effect. We investigated whether this GH secretagogue attenuates liver injury in LPS-treated rats. Wistar rats were simultaneously injected (ip) with LPS (1 mg/kg) and/or GHRP-2 (100 μg/kg). Serum levels of aspartate and alanine transaminases were measured as an index of liver damage. Circulating nitrites/nitrates and hepatic IGF-I and TNF-α were evaluated as possible mediators of GHRP-2 actions. LPS increased serum levels of transaminases and nitrites/nitrates. Moreover, LPS increased hepatic TNF-α and decreased hepatic IGF-I mRNAs. GHRP-2 administration attenuated the effects of LPS on transaminases, nitrites/nitrates, TNF-α, and IGF-I in vivo. This GHRP-2 effect does not seem to be due to modifications in food intake, since fasting did not modify serum levels of transaminases, serum nitrites/nitrates, and hepatic TNF-α mRNA both in vehicle rats and in LPS-injected rats. To elucidate whether GHRP-2 is acting directly on the liver, cocultures of hepatocytes and nonparenchymal cells and monocultures of isolated hepatocytes were incubated with LPS and GHRP-2. The ghrelin receptor agonist prevented an endotoxin-induced increase in transaminases and nitrite/nitrate release as well as in TNF-α mRNA and increased IGF-I mRNA from cocultures of hepatocytes and nonparenchymal cells, but not from monocultures. In summary, these data indicate that GHRP-2 has a protective effect on the liver in LPS-injected rats that seems to be mediated by IGF-I, TNF-α, and nitric oxide. Our data also suggest that the anti-inflammatory effect of GHRP-2 in the liver is exerted on nonparenchymal cells.

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