scholarly journals Astilbe Chinensis ethanol extract suppresses inflammation in macrophages via NF-κB pathway

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Tae-Young Gil ◽  
Bo-Ram Jin ◽  
Chul-Hee Hong ◽  
Jong Hyuk Park ◽  
Hyo-Jin An
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Cytokines ◽  
Inflammatory Mediators ◽  
Ethanol Extract ◽  
Nuclear Factor Κb ◽  
Peritoneal Macrophages ◽  
Necrosis Factor Alpha ◽  
Iκb Kinase ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Abstract Background Macrophages play a crucial role in inflammation. Astilbe chinensis is one of perennial herbs belonging to the genus Astilbe. Plants in the genus have been used for pain, headaches, arthralgia, and chronic bronchitis. However, the effect of A.chinensis on inflammation remains unclear. To study the anti-inflammatory action of A.chinensis ethanol extract (ACE), we investigated the effect of ACE on the production of pro-inflammatory mediators and cytokines in macrophages. Methods We evaluated the effectiveness of ACE in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages and thioglycollate (TG)-elicited peritoneal macrophages from male C57BL/6 mice. We measured the levels of pro-inflammatory mediators and cytokines, and examined the anti-inflammatory actions of ACE on nuclear factor κB (NF-κB) pathway in the macrophages. Western blot analysis and immunofluorescence microscopy were used to determine protein level and translocation, respectively. Results ACE suppressed the output of nitric oxide (NO), prostaglandin E2 (PGE2), and pro-inflammatory cytokines in stimulated macrophages via inhibiting the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) proteins. ACE suppressed mRNA expression of pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α). We examined the efficacies of ACE on NF-κB activation by measuring the expressions including IκB kinase (IKK), inhibitor of κB (IκB), and nuclear p65 proteins. In addition, the inhibition of NF-κB p65’s translocation was determined with immunofluorescence assay. Conclusion Our findings manifested that ACE inhibited LPS or TG-induced inflammation by blocking the NF-κB signaling pathway in macrophages. It indicated that ACE is a potential therapeutic mean for inflammation and related diseases.

Pro-inflammatory cytokines reduce human TAFI expression via tristetraprolin-mediated mRNA destabilisation and decreased binding of HuR

2015 ◽  
Vol 114 (08) ◽  
pp. 337-349 ◽  
Author(s):  
Dragana Komnenov ◽  
Corey Scipione ◽  
Zainab Bazzi ◽  
Justin Garabon ◽  
Marlys Koschinsky ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Inflammatory Mediators ◽  
Hepg2 Cells ◽  
Inflammatory Cells ◽  
Gene Encoding ◽  
Protein Levels ◽  
Anti Inflammatory ◽  
Mechanistic Basis ◽  
Pro Inflammatory Cytokines

SummaryThrombin activatable fibrinolysis inhibitor (TAFI) is the zymogen form of a basic carboxypeptidase (TAFIa) with both anti-fibrinolytic and anti-inflammatory properties. The role of TAFI in inflammatory disease is multifaceted and involves modulation both of specific inflammatory mediators as well as of the behaviour of inflammatory cells. Moreover, as suggested by in vitro studies, inflammatory mediators are capable of regulating the expression of CPB2, the gene encoding TAFI. In this study we addressed the hypothesis that decreased TAFI levels observed in inflammation are due to post-transcriptional mechanisms. Treatment of human HepG2 cells with pro-inflammatory cytokines TNFα, IL-6 in combination with IL-1β, or with bacterial lipopolysaccharide (LPS) decreased TAFI protein levels by approximately two-fold over 24 to 48 hours of treatment. Conversely, treatment of HepG2 cells with the anti-inflammatory cytokine IL-10 increased TAFI protein levels by two-fold at both time points. We found that the mechanistic basis for this modulation of TAFI levels involves binding of tristetraprolin (TTP) to the CPB2 3′-UTR, which mediates CPB2 mRNA destabilisation. In this report we also identified that HuR, another ARE-binding protein but one that stabilises transcripts, is capable of binding the CBP2 3’UTR. We found that pro-inflammatory mediators reduce the occupancy of HuR on the CPB2 3’-UTR and that the mutation of the TTP binding site in this context abolishes this effect, although TTP and HuR appear to contact discrete binding sites. Interestingly, all of the mediators tested appear to increase TAFI protein expression in THP-1 macrophages, likewise through effects on CPB2 mRNA stability.

scholarly journals Anti-Inflammatory Activity of Sonchus oleraceus Extract in Lipopoly saccharide-Stimulated RAW264.7 Cells

2018 ◽  
Vol 11 (4) ◽  
pp. 1755-1761
Author(s):  
Eun-Jin Yang ◽  
Sungchan Jang ◽  
Kwang Hee Hyun ◽  
Eun-Young Jung ◽  
Seung-Young Kim ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Cytokines ◽  
Inflammatory Activity ◽  
Raw264.7 Cells ◽  
Supporting Evidence ◽  
Dependent Manner ◽  
Sonchus Oleraceus ◽  
Raw264.7 Macrophages ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

The anti-inflammatory activity and non-toxicity of Sonchus oleraceus extract (J6) were tested by measuring its effect on the levels of nitric oxide (NO), prostaglandin E2 (PGE2), and the pro-inflammatory cytokines, interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages. We treated the RAW264.7 cells with various concentrations (50, 100, or 200 μg/mL) of J6. Our results showed that J6 inhibited the production of NO, PGE2, and pro-inflammatory cytokines in a concentration-dependent manner, without compromising cell viability. In addition, we provided supporting evidence that the inhibitory activity of J6 on the production of NO and PGE2 occurred via the downregulation of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), respectively. Our findings suggest that J6 is a new source for anti-inflammatory drugs and ingredients for healthcare products that include functional cosmetics.

scholarly journals Anti-Inflammatory Effect of Pineapple Rhizome Bromelain through Downregulation of the NF-κB- and MAPKs-Signaling Pathways in Lipopolysaccharide (LPS)-Stimulated RAW264.7 Cells

2021 ◽  
Vol 43 (1) ◽  
pp. 93-106
Author(s):  
Orapin Insuan ◽  
Phornphimon Janchai ◽  
Benchaluk Thongchuai ◽  
Rujirek Chaiwongsa ◽  
Supaporn Khamchun ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Inflammatory Cytokines ◽  
Molecular Mechanisms ◽  
Raw264.7 Cells ◽  
Nuclear Factor ◽  
Amino Terminal ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Bromelain is a mixture of proteolytic enzymes derived from pineapple (Ananas comosus) fruit and stem possessing several beneficial properties, particularly anti-inflammatory activity. However, the molecular mechanisms underlying the anti-inflammatory effects of bromelain are unclear. This study investigated the anti-inflammatory effects and inhibitory molecular mechanisms of crude and purified rhizome bromelains on lipopolysaccharide (LPS)-induced inflammation in RAW 264.7 macrophage cells. RAW264.7 cells were pre-treated with various concentrations of crude bromelain (CB) or purified bromelain (PB), and then treated with LPS. The production levels of pro-inflammatory cytokines and mediators, including nitric oxide (NO), interleukin (IL)-6, and tumor necrosis factor (TNF)-α were determined by Griess and ELISA assays. The expressions of inducible nitric oxide synthetase (iNOS), cyclooxygenase (COX)-2, nuclear factor kappa B (NF-κB), and mitogen-activated protein kinases (MAPKs)-signaling pathway-related proteins were examined by western blot analysis. The pre-treatment of bromelain dose-dependently reduced LPS-induced pro-inflammatory cytokines and mediators, which correlated with downregulation of iNOS and COX-2 expressions. The inhibitory potency of PB was stronger than that of CB. PB also suppressed phosphorylated NF-κB (p65), nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor alpha, extracellular signal-regulated kinases, c-Jun amino-terminal kinases, and p38 proteins in LPS-treated cells. PB then exhibited potent anti-inflammatory effects on LPS-induced inflammatory responses in RAW264.7 cells by inhibiting the NF-κB and MAPKs-signaling pathways.

Fisetin has Inhibitory Effects on the TLR 4/NF-κB-Mediated Inflammatory Pathway After Traumatic Brain Injury in Mice: A Potential Neuroprotective Role

2021 ◽  
Author(s):  
Chenhui Zhou ◽  
Sheng Nie ◽  
Zhepei Wang ◽  
Fanyong Gong ◽  
Jingmi Wu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Edema ◽  
Inflammatory Cytokines ◽  
Nuclear Factor Κb ◽  
Neuroprotective Effects ◽  
Inflammatory Pathway ◽  
Mortality And Morbidity ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Abstract Inflammatory response contributes to the high mortality and morbidity of traumatic brain injury (TBI). Potent anti-inflammatory effects can alleviate brain injury after TBI. Fisetin has anti-inflammatory properties in several brain injury models, but the effects of fisetin on inflammation after TBI is still unclear. Our study aimed to investigate the neuroprotective effects of fisetin against inflammation after TBI in mice.Fisetin (25 mg/kg, 50 mg/kg or 75 mg/kg) or equal volume of vehicle was given via intraperitoneal injection 30 min after TBI. The neurological severity score, brain edema and blood brain barrier (BBB) permeability were assayed after TBI. In further mechanistic studies, changes in the toll-like receptor 4 (TLR 4)/nuclear factor-κB (NF-κB) pathway and the expression of pro-inflammatory cytokines were measured. Fisetin significantly improved behavioral outcomes and reduced brain edema after TBI. These changes were associated with significant reductions in TLR 4 expression and NF-κB activity. In addition, changes in the expression of pro-inflammatory cytokines were detected 24 h after TBI. Our study provided the first evidence that fisetin exerted neuroprotective effects by inhibiting the TLR 4/NF-κB–mediated inflammatory pathway after TBI in mice.

Anti-Inflammatory Activity of Hyperoside Through the Suppression of Nuclear Factor-κB Activation in Mouse Peritoneal Macrophages

2011 ◽  
Vol 39 (01) ◽  
pp. 171-181 ◽  
Author(s):  
Su-Jin Kim ◽  
Jae-Young Um ◽  
Seung-Heon Hong ◽  
Ju-Young Lee
Keyword(s):  
Nitric Oxide ◽  
Tumor Necrosis Factor ◽  
Interleukin 6 ◽  
Tumor Necrosis ◽  
Nuclear Factor Κb ◽  
Peritoneal Macrophages ◽  
Nuclear Factor ◽  
Anti Inflammatory ◽  
Mouse Peritoneal Macrophages ◽  
Necrosis Factor

Hyperoside (quercetin-3-O-galactoside) is a flavonoid compound mainly found in the herb plants Hypericum perforatum L and Crataegus pinnatifida. Although hyperoside has a variety of pharmacological effects including anti-viral, anti-oxidative, and anti-apoptotic activities, the anti-inflammatory mechanism of hyperoside in mouse peritoneal macrophages remains unclear. In this study, hyperoside was shown to exert an anti-inflammatory action through suppressed production of tumor necrosis factor, interleukin-6, and nitric oxide in lipopolysaccharide-stimulated mouse peritoneal macrophages. The maximal inhibition rate of tumor necrosis factor-α, interleukin-6, and nitric oxide production by 5 μM hyperoside was 32.31 ± 2.8%, 41.31 ± 3.1%, and 30.31 ± 4.1%, respectively. In addition, hyperoside inhibited nuclear factor-κB activation and IκB-α degradation. The present study suggests that an important molecular mechanism by hyperoside reduces inflammation, which might explain its beneficial effect in the regulation of inflammatory reactions.

scholarly journals Anti-Inflammatory Effects of 6-Methylcoumarin in LPS-Stimulated RAW 264.7 Macrophages via Regulation of MAPK and NF-κB Signaling Pathways

Molecules ◽  
2021 ◽  
Vol 26 (17) ◽  
pp. 5351
Author(s):  
Jin-Kyu Kang ◽  
You-Chul Chung ◽  
Chang-Gu Hyun
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Cytokines ◽  
Mitogen Activated Protein Kinase ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Persistent inflammatory reactions promote mucosal damage and cause dysfunction, such as pain, swelling, seizures, and fever. Therefore, in this study, in order to explore the anti-inflammatory effect of 6-methylcoumarin (6-MC) and suggest its availability, macrophages were stimulated with lipopolysaccharide (LPS) to conduct an in vitro experiment. The effects of 6-MC on the production and levels of pro-inflammatory cytokines (interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α) and inflammatory mediators (nitric oxide (NO), prostaglandin E2 (PGE2)) in LPS-stimulated RAW 264.7 cells were examined. The results showed that 6-MC reduced the levels of NO and PGE2 without being cytotoxic. In addition, it was demonstrated that the increase in the expression of pro-inflammatory cytokines caused by LPS stimulation, was decreased in a concentration-dependent manner with 6-MC treatment. Moreover, Western blot results showed that the protein levels of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), which increased with LPS treatment, were decreased by 6-MC treatment. Mechanistic studies revealed that 6-MC reduced the phosphorylation of the mitogen-activated protein kinase (MAPK) family and IκBα in the MAPK and nuclear factor-kappa B (NF-κB) pathways, respectively. These results suggest that 6-MC is a potential therapeutic agent for inflammatory diseases that inhibits inflammation via the MAPK and NF-κB pathways.

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