Molecular mechanisms of anti-inflammatory action of glucocorticoids

BioEssays ◽  
1996 ◽  
Vol 18 (5) ◽  
pp. 371-378 ◽  
Author(s):  
Andrew C. B. Cato ◽  
Erik Wade
Keyword(s):  
Molecular Mechanisms ◽  
Anti Inflammatory ◽  
Inflammatory Action

scholarly journals The Involvement of PPARγ In Anti-Inflammatory Activity of N-Stearoylethanolamide

2021 ◽  
Author(s):  
Halyna Kosiakova ◽  
Andrii Berdyshev ◽  
Victor Dosenko ◽  
Tetyana Drevytska ◽  
Oleksandra Herasymenko ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Ex Vivo ◽  
Methodological Approach ◽  
Mrna Level ◽  
Peritoneal Macrophages ◽  
Insulin Resistant ◽  
Wide Range ◽  
Anti Inflammatory ◽  
Pre Treatment ◽  
Inflammatory Action

Abstract N-stearoylethanolamide (NSE)– a cannabinoid-like compound with wide range of biological activity. Anti-inflammatory properties of NSE have been indicated on different animal models of pathological conditions. However, the molecular mechanisms of anti-inflammatory action of NSE remain unclear. In the current study, the involvement of PPARγ in the NF-kB -dependent anti-inflammatory action of NSE was evaluated using different methodological approach. First method - molecular modeling, evaluated the possibility of NSE to bind with PPAR. Then, in ex vivo experiment, using selective synthetic agonist of PPARα/γ LY-171883 and selective antagonist of PPARγ - GW9662, the role of PPARα /PPARγ in the NSE’s effect on nuclear NF-kB translocation was examined in LPS-activated rat peritoneal macrophages. Finally, the NSE action on the mRNA level of several PPARγ- dependent genes was studied in liver of insulin-resistant rats. The molecular docking results showed that NSE could bind to PPARγ and compete for the binding with antagonist GW9662 and agonist LY171883 in the active site of PPARγ. It also has been found that NSE prevented the LPS-induced NF-kB translocation into the nuclei of rat peritoneal macrophages during pre-treatment with NSE before LPS application. When NSE was added before GW9662 and LPS treatment, the level of NF-kB translocation and IL-1β content reduced to control cells’ levels. These data confirmed a competitive binding of NSE with GW9662 for the ligand-binding domen of PPARγ. In addition, NSE administration to insulin resistant rats changed the mRNA expression of several PPARγ target gens, including FATP1 and IL1-ra.

scholarly journals HDAC2 is required by the physiological concentration of glucocorticoid to inhibit inflammation in cardiac fibroblasts

2017 ◽  
Vol 95 (9) ◽  
pp. 1030-1038 ◽  
Author(s):  
Haining Zhang ◽  
Yanhua He ◽  
Guiping Zhang ◽  
Xiaobin Li ◽  
Suikai Yan ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Cardiac Fibroblasts ◽  
Myocardial Inflammation ◽  
Physiological Concentration ◽  
Physiological Level ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Inflammatory Action

We previously suggested that endogenous glucocorticoids (GCs) may inhibit myocardial inflammation induced by lipopolysaccharide (LPS) in vivo. However, the possible cellular and molecular mechanisms were poorly understood. In this study, we investigated the role of physiological concentration of GCs in inflammation induced by LPS in cardiac fibroblasts and explored the possible mechanisms. The results showed that hydrocortisone at the dose of 127 ng/mL (equivalent to endogenous basal level of GCs) inhibited LPS (100 ng/mL)-induced productions of TNF-α and IL-1β in cardiac fibroblasts. Xanthine oxidase/xanthine (XO/X) system impaired the anti-inflammatory action of GCs through downregulating HDAC2 activity and expression. Knockdown of HDAC2 restrained the anti-inflammatory effects of physiological level of hydrocortisone, and blunted the ability of XO/X system to downregulate the inhibitory action of physiological level of hydrocortisone on cytokines. These results suggested that HDAC2 was required by the physiological concentration of GC to inhibit inflammatory response. The dysfunction of HDAC2 induced by oxidative stress might be account for GC resistance and chronic inflammatory disorders during the cardiac diseases.

scholarly journals Anti-Inflammatory Effects of Berberine Hydrochloride in an LPS-Induced Murine Model of Mastitis

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Xichun Wang ◽  
Shibin Feng ◽  
Nana Ding ◽  
Yanting He ◽  
Cheng Li ◽  
...  
Keyword(s):  
Murine Model ◽  
Molecular Mechanisms ◽  
Neutrophil Infiltration ◽  
Mammary Glands ◽  
Histopathological Changes ◽  
Berberine Hydrochloride ◽  
Treatment Groups ◽  
Qrt Pcr ◽  
Anti Inflammatory ◽  
Inflammatory Action

Berberine hydrochloride is an isoquinoline type alkaloid extracted from Berberidaceae, Rutaceae, and other plants. Previous reports have shown that berberine hydrochloride has anti-inflammatory properties. However, the underlying molecular mechanisms remain unclear. In this study, a lipopolysaccharide- (LPS-) induced murine model of mastitis was established to explore the anti-inflammatory action of berberine hydrochloride. Sixty mice that had been lactating for 5–7 days were randomly divided into six groups, including control, LPS, three berberine hydrochloride treatment groups (5, 10, and 20 mg/kg), and a dexamethasone (DEX) (5 mg/kg) group. Berberine hydrochloride was administered intraperitoneally 1 h before and 12 h after LPS-induced mastitis, and all mice were sacrificed 24 h after LPS induction. The pathological and histopathological changes of the mammary glands were observed. The concentrations and mRNA expressions of TNF-α, IL-1β, and IL-6 were measured by ELISA and qRT-PCR. The activation of TLR4 and NF-κB signaling pathways was analyzed by Western blot. Results indicated that berberine hydrochloride significantly attenuated neutrophil infiltration and dose-dependently decreased the secretion and mRNA expressions of TNF-α, IL-1β, and IL-6 within a certain range. Furthermore, berberine hydrochloride suppressed LPS-induced TLR4 and NF-κB p65 activation and the phosphorylation of I-κB. Berberine hydrochloride can provide mice robust protection from LPS-induced mastitis, potentially via the TLR4 and NF-κB pathway.

scholarly journals Molecular Mechanisms of Anti-Inflammatory Action of Erythromycin in Human Bronchial Epithelial Cells: Possible Role in the Signaling Pathway That Regulates Nuclear Factor-κB Activation

2004 ◽  
Vol 48 (5) ◽  
pp. 1581-1585 ◽  
Author(s):  
Masashi Desaki ◽  
Hitoshi Okazaki ◽  
Toshiaki Sunazuka ◽  
Satoshi Omura ◽  
Kazuhiko Yamamoto ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Nuclear Factor Κb ◽  
Bronchial Epithelial Cells ◽  
Nuclear Factor ◽  
Human Bronchial Epithelial Cells ◽  
Bronchial Epithelial ◽  
Anti Inflammatory ◽  
Inflammatory Action

ABSTRACT Long-term macrolide therapy has been proven to improve survival in patients with diffuse panbronchiolitis. Although its mechanisms remain unknown, previous studies have suggested the effects of macrolide might be anti-inflammatory rather than antibacterial. To elucidate the molecular mechanisms of its action, we studied here the effects of erythromycin (EM) and its new derivative, EM703, which shows no antibacterial action, on the activation of the transcription factor nuclear factor-κB (NF-κB) in human bronchial epithelial cells. Western blotting analysis showed that EM did not inhibit the degradation of IκBα, suggesting the molecular target for EM was not the dissociation of NF-κB from IκB. An electrophoretic mobility shift assay showed that EM did not interrupt the NF-κB DNA-binding activity in the nucleus under the conditions tested. Moreover, not only EM but also EM703 suppressed the activation of NF-κB and the production of interleukin-8, demonstrating that the anti-inflammatory action of the macrolide is independent of its antibacterial activity. Taken together, these data suggest EM has an anti-inflammatory action, presumably via an interaction with the NF-κB signaling pathway in the downstream of the dissociation from IκB, resulting in the inhibition of NF-κB.

An emphasis on molecular mechanisms of anti-inflammatory effects and glucocorticoid resistance

2015 ◽  
Vol 12 (1) ◽  
pp. 1-13 ◽  
Author(s):  
Deepa K. Ingawale ◽  
Satish K. Mandlik ◽  
Snehal S. Patel
Keyword(s):  
Molecular Mechanisms ◽  
Inflammatory Diseases ◽  
Platelet Activating Factor ◽  
Enzyme Modulation ◽  
New Strategy ◽  
Acid Metabolites ◽  
Inflammatory Proteins ◽  
Anti Inflammatory ◽  
Therapeutic Problem ◽  
Inflammatory Action

AbstractGlucocorticoids (GC) are universally accepted agents for the treatment of anti-inflammatory and immunosuppressive disorders. They are used in the treatment of rheumatic diseases and various inflammatory diseases such as allergy, asthma and sepsis. They bind with GC receptor (GR) and form GC–GR complex with the receptor and exert their actions. On activation the GC–GR complex up-regulates the expression of nucleus anti-inflammatory proteins called as transactivation and down-regulates the expression of cytoplasmic pro-inflammatory proteins called as transrepression. It has been observed that transactivation mechanisms are notorious for side effects and transrepressive mechanisms are identified for beneficial anti-inflammatory effects of GC therapy. GC hampers the function of numerous inflammatory mediators such as cytokines, chemokines, adhesion molecules, arachidonic acid metabolites, release of platelet-activating factor (PAF), inflammatory peptides and enzyme modulation involved in the process of inflammation. The GC resistance is a serious therapeutic problem and limits the therapeutic response of GC in chronic inflammatory patients. It has been observed that the GC resistance can be attributed to cellular microenvironment changes, as a consequence of chronic inflammation. Various other factors responsible for resistance have been identified, including alterations in both GR-dependent and GR-independent signaling pathways of cytokine action, hypoxia, oxidative stress, allergen exposure and serum-derived factors. The present review enumerates various aspects of inflammation such as use of GC for treatment of inflammation and its mechanism of action. Molecular mechanisms of anti-inflammatory action of GC and GC resistance, alternative anti-inflammatory treatments and new strategy for reversing the GC resistance have also been discussed.

scholarly journals Anticancer and Anti-Inflammatory Effects of Tomentosin: Cellular and Molecular Mechanisms

Separations ◽  
2021 ◽  
Vol 8 (11) ◽  
pp. 207
Author(s):  
Nasreddine El Omari ◽  
Naoual El Menyiy ◽  
Gokhan Zengin ◽  
Bey Hing Goh ◽  
Monica Gallo ◽  
...  
Keyword(s):  
Natural Compound ◽  
Molecular Mechanisms ◽  
Cancer Disease ◽  
Close Link ◽  
Starting Point ◽  
Anti Inflammatory ◽  
Asteraceae Family ◽  
Potential Cancer ◽  
Different Levels ◽  
Inflammatory Action

Tomentosin is a natural compound known for its presence in some medicinal plants of the Asteraceae family such as Inula viscosa. Recent studies have highlighted its anticancer and anti-inflammatory properties. Its anticancer mechanisms are unique and act at different levels ranging from cellular organization to molecular transcriptional factors and epigenetic modifications. Tomentosin’s possession of the modulatory effect on telomerase expression on tumor cell lines has captured the interest of researchers and spurred a more robust study on its anticancer effect. Since inflammation has a close link with cancer disease, this natural compound appears to be a potential cancer-fighting drug. Indeed, its recently demonstrated anti-inflammatory action can be considered as a starting point for its evaluation as an anticancer chemo-preventive agent

Bioguided determination of the anti-inflammatory action of STW 5 and STW 6

Planta Medica ◽  
2008 ◽  
Vol 74 (09) ◽  
Author(s):  
K Nieber ◽  
S Michael ◽  
K Grötzinger ◽  
JW Rauwald ◽  
SN Okpanyi ◽  
...  
Keyword(s):  
Anti Inflammatory ◽  
Inflammatory Action

Evaluation of anti-pyretic activity of Dracaena sanderiana by Brewer’s yeast method

2020 ◽  
Vol 9 (2) ◽  
pp. 32-34
Author(s):  
Pavani C H
Keyword(s):  
Herbal Remedies ◽  
Standard Drug ◽  
Chemical Substances ◽  
Beneficial Effects ◽  
Potential Value ◽  
Plant Effects ◽  
Therapeutic Properties ◽  
Dracaena Sanderiana ◽  
Anti Inflammatory ◽  
Inflammatory Action

These medicinal plants are used to develop a therapy for the disease. To improve the science, investigate the scientific proof and activities validation, therefore the use of various herbal remedies for their pain-relieving and anti-inflammatory action in these current days. includes influence, anti-inflammatory, anti effect, analgesia, effects and some beneficial effects on the GI system. show the potential value of pain relief, cancer prevention and weight loss. According to these plant effects, consider that this present study was mainly based on to investigate and likely to reduce the fever caused by the outdoor and indoor. potential of is evidenced in leave studies. The medicinal plant produces a variety of chemical substances which shows significant therapeutic properties with the standard drug paracetamol.

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