scholarly journals Butanol extracts of Asparagus?cochinchinensis fermented with Weissella?cibaria inhibit iNOS‑mediated COX‑2 induction pathway and inflammatory cytokines in LPS‑stimulated RAW264.7 macrophage cells

2017 ◽  
Author(s):  
Hyun Lee ◽  
Bo Song ◽  
Hye Kim ◽  
Ji Kim ◽  
Woo Yun ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Weissella Cibaria ◽  
Macrophage Cells ◽  
Cox 2 ◽  
Asparagus Cochinchinensis ◽  
Raw264.7 Macrophage

Puerarin inhibits iNOS, COX-2 and CRP expression via suppression of NF-κB activation in LPS-induced RAW264.7 macrophage cells

2011 ◽  
Vol 63 (3) ◽  
pp. 781-789 ◽  
Author(s):  
Wenzhi Hu ◽  
Xiangjun Yang ◽  
Cao Zhe ◽  
Qin Zhang ◽  
Lie Sun ◽  
...  
Keyword(s):  
Macrophage Cells ◽  
Cox 2 ◽  
Raw264.7 Macrophage

scholarly journals N-Butanol Extract of Gastrodia elata Suppresses Inflammatory Responses in Lipopolysaccharide-Stimulated Macrophages and Complete Freund’s Adjuvant- (CFA-) Induced Arthritis Rats via Inhibition of MAPK Signaling Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-11
Author(s):  
Peng He ◽  
Yiwen Hu ◽  
Changzhao Huang ◽  
Xi Wang ◽  
Heng Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Therapeutic Effect ◽  
Inflammatory Cytokines ◽  
Gastrodia Elata ◽  
Butanol Extract ◽  
Freund’S Adjuvant ◽  
Cox 2 ◽  
Freund's Adjuvant ◽  
Anti Inflammatory ◽  
Raw264.7 Macrophage

Gastrodia elata is a traditional herbal medicine that has been used for centuries to treat rheumatism. Previous studies have confirmed that ethanol extracts of Gastrodia elata have anti-inflammatory and antioxidant activities, and the n-butanol fraction exerts a higher inhibitory effect. However, the in vivo anti-inflammatory effects of Gastrodia elata have not been evaluated. Thus, we assessed the therapeutic effect of the n-butanol extract of Gastrodia elata (BGE) on complete Freund’s adjuvant- (CFA-) induced arthritis rats which were separated into six groups (NOR; MODEL; CFA + dexamethasone (DEX); CFA + 25, 50, 100 mg/kg BGE). The paw swelling, joint radiology, and histology were used to analyze the effect of BGE on delaying the progression of rheumatoid arthritis. Furthermore, serum levels of inflammatory cytokines were analyzed via ELISA. In addition, the effect of BGE on nitric oxide (NO) production, expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2(COX-2), and inflammatory cytokines were detected in lipopolysaccharide- (LPS-) stimulated RAW264.7 macrophage cells. Lastly, the impacts of BGE on the activation of the mitogen-activated protein kinases (MAPK) pathway in CFA rats and LPS-stimulated RAW264.7 macrophage were examined by western blot analysis. The results show that BGE can significantly reduce paw swelling without losing the body weight of rats. Imaging assessment confirms that BGE can protect cartilage from destruction, as well as reducing inflammatory cell infiltration and synovial proliferation. Moreover, BGE suppresses the production of inflammatory cytokines in serum and inhibits the activation of the phosphorylation of p38 and ERK in CFA rats. BGE was also demonstrated to decrease the production of NO and inflammatory cytokines in LPS-stimulated RAW264.7 cells. The effect of BGE in LPS-induced expression leads to reduced p38 and ERK phosphorylation and also downregulates the protein expression of iNOS and COX-2. Taken together, BGE exhibits a potential therapeutic effect on CFA rats, and its anti-inflammatory and antioxidant effects were possibly exerted by regulation of ERK/p38MAPK.

Mitragynine inhibits the COX-2 mRNA expression and prostaglandin E2 production induced by lipopolysaccharide in RAW264.7 macrophage cells

2011 ◽  
Vol 136 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Zulkhurnain Utar ◽  
Mohamed Isa Abdul Majid ◽  
Mohd Ilham Adenan ◽  
Mohd Fadzly Amar Jamil ◽  
Tan Mei Lan
Keyword(s):  
Prostaglandin E2 ◽  
Mrna Expression ◽  
Macrophage Cells ◽  
Cox 2 ◽  
Raw264.7 Macrophage

scholarly journals Ameliorative Effects of Cardamonin on Monosodium Urate-Induced Gouty Arthritis through Inhibiting NLRP3 Inflammasome Mediation

Medicina ◽  
2021 ◽  
Vol 57 (9) ◽  
pp. 898
Author(s):  
Chih-Chien Wang ◽  
Jeng-Wei Lu ◽  
Yi-Jen Peng ◽  
Chian-Her Lee ◽  
Herng-Sheng Lee ◽  
...  
Keyword(s):  
Inflammatory Cytokines ◽  
Nlrp3 Inflammasome ◽  
Gouty Arthritis ◽  
Inflammasome Activation ◽  
Monosodium Urate ◽  
In Vivo Models ◽  
Macrophage Cells ◽  
Caspase 1 ◽  
Cox 2

Background and Objectives: Gouty arthritis is an acute inflammatory response caused by the precipitation of monosodium urate (MSU) crystals in joints. The triggering of MSU leads to increased production of inflammatory cytokines, such as interleukin-1β, which in turn lead to the formation of macromolecular complexes, referred to as inflammasomes. Thorough characterization of the NLRP3 inflammasome can be used as an indicator of an immune response against harmful stimuli. Cardamonin is a chalcone, mainly found in the seeds of Alpinia katsumadai, and exhibits anti-inflammatory activity by inhibiting the release of pro-inflammatory cytokines in vitro. However, the mechanism by which cardamonin treatment alleviates gouty arthritis has yet to be fully elucidated. Materials and Methods: In vitro or in vivo models were used to study whether cardamonimn inhibited NLRP3 inflammasome activation or suppressed gouty inflammation. Results: In the current study, we determined that most NLRP3 was released passively after MSU stimulation, and this release of NLRP3 promoted caspase-1 activation and IL-1β secretion. Cardamonin was shown to decrease both the activity of caspase-1 and secretion of IL-1β in J774A.1 macrophage cells subjected to MSU stimulation. Cardamonin was also shown to attenuate the production of COX-2 in MSU-stimulated J774A.1 macrophage cells. Finally, cardamonin reduced the thickness of the synovial lining and the infiltration of gouty arthritis in a rat model. Conclusions: Overall, cardamonin significantly attenuated IL-1β secretion, caspase-1 activity, and COX-2 production stimulated by MSU. These findings provide new insights into the molecular mechanisms underlying the effects of cardamonin treatment for gouty arthritis.

Long Noncoding RNA SNHG1 Promotes Lipopolysaccharide-Induced Activation and Inflammation in Microglia via Targeting miR-181b

2021 ◽  
pp. 1-11
Author(s):  
Jun Dong ◽  
Tingkai Fu ◽  
Yunxue Yang ◽  
Zhenxin Mu ◽  
Xingang Li
Keyword(s):  
Inflammatory Cytokines ◽  
Long Noncoding Rna ◽  
Calcium Binding ◽  
Noncoding Rna ◽  
Morphological Changes ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammation Response ◽  
Tnf Α ◽  
Cox 2

<b><i>Introduction:</i></b> Long noncoding RNA small nuclear host gene 1 (SNHG1) was involved in neuroinflammation in microglial BV-2 cells; however, its interaction with microRNA (miR)-181b in lipopolysaccharide (LPS)-induced BV-2 cells remained poor. <b><i>Methods:</i></b> BV-2 cells were treated with LPS and then were subjected to observation on morphology and immunofluorescence staining. After transfection, levels of inflammatory cytokines interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) were determined with enzyme-linked immunosorbent assay (ELISA). The potential binding sites between SNHG1 and miR-181b were confirmed using dual-luciferase reporter assay. Quantitative real-time polymerase chain reaction and Western blot were applied for detecting the mRNA and protein expressions of proinflammatory cytokines, ionized calcium-binding adapter molecule 1 (Iba1), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). <b><i>Results:</i></b> LPS led to the morphological changes and activation of BV-2 cells. The transfection of SNHG1 overexpression vector further promoted LPS-induced SNHG1 upregulation, inflammatory cytokines (IL-1β, IL-6, and TNF-α) generation and Iba-1, COX-2, and iNOS expressions, whereas silencing SNHG1 did the opposite. miR-181b functions as a downstream miRNA of SNHG1. In LPS-treated cells, the inhibition of miR-181b induced by SNHG1 promoted inflammation response and the expressions of Iba-1, COX-2, and iNOS. <b><i>Conclusion:</i></b> SNHG1 was involved in LPS-induced microglial activation and inflammation response via targeting miR-181b, providing another evidence of the roles of SNHG1 implicated in neuroinflammation of microglia.

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