scholarly journals Anti-inflammatory effects of Salvia plebeia R. Br extract in vitro and in ovalbumin-induced mouse model

2016 ◽  
Vol 49 (1) ◽  
Author(s):  
Hwan-Hee Jang ◽  
Su-Yeon Cho ◽  
Mi-Ju Kim ◽  
Jung-Bong Kim ◽  
Sung-Hyen Lee ◽  
...  
Keyword(s):  
Mouse Model ◽  
Anti Inflammatory

scholarly journals Modulation of Glial Responses by Furanocembranolides: Leptolide Diminishes Microglial Inflammation in Vitro and Ameliorates Gliosis In Vivo in a Mouse Model of Obesity and Insulin Resistance

Marine Drugs ◽  
2020 ◽  
Vol 18 (8) ◽  
pp. 378
Author(s):  
Miriam Corraliza-Gómez ◽  
Amalia B. Gallardo ◽  
Ana R. Díaz-Marrero ◽  
José M. de la Rosa ◽  
Luis D’Croz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Microglial Cells ◽  
Obese Mouse ◽  
Neurodegenerative Process ◽  
Age Related ◽  
Bv2 Cells ◽  
Anti Inflammatory ◽  
Inflammatory Molecules

Neurodegenerative diseases are age-related disorders caused by progressive neuronal death in different regions of the nervous system. Neuroinflammation, modulated by glial cells, is a crucial event during the neurodegenerative process; consequently, there is an urgency to find new therapeutic products with anti-glioinflammatory properties. Five new furanocembranolides (1−5), along with leptolide, were isolated from two different extracts of Leptogorgia sp., and compound 6 was obtained from chemical transformation of leptolide. Their structures were determined based on spectroscopic evidence. These seven furanocembranolides were screened in vitro by measuring their ability to modulate interleukin-1β (IL-1β) production by microglial BV2 cells after LPS (lipopolysaccharide) stimulation. Leptolide and compounds 3, 4 and 6 exhibited clear anti-inflammatory effects on microglial cells, while compound 2 presented a pro-inflammatory outcome. The in vitro results prompted us to assess anti-glioinflammatory effects of leptolide in vivo in a high-fat diet-induced obese mouse model. Interestingly, leptolide treatment ameliorated both microgliosis and astrogliosis in this animal model. Taken together, our results reveal a promising direct biological effect of furanocembranolides on microglial cells as bioactive anti-inflammatory molecules. Among them, leptolide provides us a feasible therapeutic approach to treat neuroinflammation concomitant with metabolic impairment.

scholarly journals OP0174 POLYDATIN PREVENTS CALCIUM PYROPHOSPHATE CRYSTAL-INDUCED ARTHRITIS IN MICE

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 108.1-109
Author(s):  
F. Oliviero ◽  
F. Galuppini ◽  
A. Scanu ◽  
P. Galozzi ◽  
V. Lazzarin ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Mouse Model ◽  
Prophylactic Treatment ◽  
Histological Analysis ◽  
Calcium Pyrophosphate ◽  
Cell Infiltrate ◽  
Therapeutic Protocol ◽  
Anti Inflammatory ◽  
Crystal Induced Arthritis

Background:Acute calcium pyrophosphate (CPP) crystal-induced inflammation is characterized by the massive release of cytokines and pro-inflammatory mediators and, from a clinical point of view, pain and limited joint function. Contrary to the precipitation of urate crystals that can be prevented through the use of hypouricemic drugs, there is no pharmacological therapy that can prevent the formation of pyrophosphate crystals.Polydatin (PD),a natural precursor of resveratrol, is a stilbenoid mainly contained in grape juice and bark of Polygonum Cuspidate. Its antioxidant, anti-inflammatory and immunomodulating properties have been demonstrated in several experimental models. We have recently shown that this compound is able to prevent the inflammatory response to pathogenic crystals in vitro (1).Objectives:The aim of this study was to assess the anti-inflammatory preventing effect of polydatin in the mouse model of acute crystal-induced arthritis.Methods:A suspension of sterile CPP crystals (0.3 mg/20 μL PBS) have been injected intra-articularly (i.a.) into one ankle joint of Balb/c mice under isoflurane anesthesia. Animals were randomized in 5 groups: 1- CPP injection, 2- CPP + PD, 3- CPP + colchicine (control drug), 4- CPP + vehicle (control. N 1), 5- PBS injection (control N. 2). Polydatin and colchicine were administered by gavage (respectively 40 mg/kg and 1mg/kg in 200 μL PBS/EtOH/glucose) at 24, 15 and 1 h before and 1, 6 and 24 h after (prophylactic model) or 1, 6 and 24 h after (therapeutic model) i.a. injection of CPP crystals.Ankle swelling was measured at different time points using a precision caliper. After 48h (peak of the acute phase) mice were euthanized and blood and ankle joints were collected for inflammatory cytokine (IL-1ß and KC) determination and histological analysis, respectively.Results:The mean change in ankle swelling after i.a injection was 0.595±0.434 mm. Prophylactic treatment with PD and colchicine significantly diminished ankle swelling to 0.175±0.115 mm and 0.137±0.100 mm, respectively (Kruskal Wallis p 0.0025; Dunn’s post test p < 0.01 CPP vs PD+CPP). The therapeutic administration of PD did not have significant effects on delta swelling (0.468±0.372 mm - PD vs 0.243±0.152 mm - colchicine). In mice treated with CPP crystals, histological analysis revealed areas of edema and increased cell infiltrate in articular and periarticular tissues and the presence of reactive lymphnodes. Tissue necrosis around inflamed tissue has been observed. Treatment with PD importantly reduced cell infiltrate in the prophylactic but not in the therapeutic protocol.Serum IL-1ß and KC levels, which increased significantly (p<0.05) after 48h from i.a injection, diminished in non significant manner after prophylactic and therapeutic treatment. The gene expression study revealed a reduction of IL-1ß and KC mRNA after PD and colchicine treatment in both groups.Conclusion:PD can effectively prevent acute inflammatory response to crystals in the mouse model of CPP arthritis. Oral PD prophylactic treatment showed a similar effect of colchicine in reducing ankle swelling and cell infiltrate. However, only colchicine showed to be effective in the therapeutic protocol.These results raise the possibility that PD might have utility in the prevention of crystal-induced acute attacks in humans.References:[1]Oliviero F, et al. Polydatin and resveratrol inhibit the inflammatory process induced by urate and pyrophosphate crystals in thp-1 cells.Foods 2019 Nov 7;8(11). pii: E560.Disclosure of Interests:Francesca Oliviero: None declared, Francesca Galuppini: None declared, Anna Scanu: None declared, Paola Galozzi: None declared, Vanni Lazzarin: None declared, Paolo Sfriso: None declared, Gianpietro Ravagnan: None declared, Roberta Ramonda Speakers bureau: Novartis, Celgene, Janssen, Pfizer, Abbvie, Lilly, Paolo Spinella: None declared, LEONARDO PUNZI: None declared, Gianmaria Pennelli: None declared, Roberto Luisetto: None declared

scholarly journals Acyclic Triterpenoid Isolated from Alpinia katsumadai Alleviates Formalin-Induced Chronic Mouse Paw Inflammation by Inhibiting the Phosphorylation of ERK and NF-κB

Molecules ◽  
2020 ◽  
Vol 25 (15) ◽  
pp. 3345 ◽  
Author(s):  
Hyung Jin Lim ◽  
Seon Gyeong Bak ◽  
Hee Ju Lim ◽  
Seung Woong Lee ◽  
Soyoung Lee ◽  
...  
Keyword(s):  
Mouse Model ◽  
Inflammatory Diseases ◽  
Extracellular Signal ◽  
Tnf Α ◽  
J774 Cells ◽  
Inflammatory Bowel ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Necrosis Factor

Chronic and excessive inflammation can destroy host organs and cause inflammatory diseases such as inflammatory bowel disease, asthma, and rheumatoid arthritis. In this study, we investigated the anti-inflammatory effects of Alpinia katsumadai seed-derived 2,3,5,22,23-pentahydroxy-2,6,10,15,19,23-hexamethyl-tetracosa-6,10,14,18-tetraene (PHT) using lipopolysaccharide (LPS)-stimulated J774 cells and a formalin-induced chronic paw inflammation mouse model. The in vitro results showed that PHT exhibited no cytotoxicity and decreased LPS-induced NO secretion. Additionally, PHT inhibited LPS-induced inducible NO synthase (iNOS) and cyclooxygenase 2 (COX2) protein expression. The quantitative real-time PCR results showed that PHT downregulated the gene expression of the proinflammatory cytokines interleukin-1β (IL-1β) and interleukin-6 (IL-6) but not tumor necrosis factor α (TNF-α). PHT inhibited the LPS-induced phosphorylation of extracellular signal-regulated kinase (ERK) and nuclear factor kappa light chain enhancer of activated B cells (NF-κB). In a mouse model, oral administration of 50 mg/kg PHT significantly alleviated both mouse paw thickness and volume. These results indicate that PHT has potential anti-inflammatory effects and should be considered a possible functional material.

scholarly journals Toxicity and Anti-inflammatory Activities of an Extract of the Eleutherine bulbosa Rhizome on Collagen Antibody-induced Arthritis in a Mouse Model

2018 ◽  
Vol 13 (7) ◽  
pp. 1934578X1801300
Author(s):  
Pham Thi Bich Hanh ◽  
Do Thi Thao ◽  
Nguyen Thi Nga ◽  
Ngo Thi Phuong ◽  
Le Ngoc Hung ◽  
...  
Keyword(s):  
Mouse Model ◽  
Ethanol Extract ◽  
Serum Levels ◽  
Negative Control ◽  
High Dose ◽  
Necrosis Factor Alpha ◽  
Beneficial Effects ◽  
Anti Inflammatory

As a continuation of our interest in the anti-inflammatory activities of Vietnamese plants, we searched for novel anti-inflammatory agents in Eleutherine bulbosa and evaluated the anti-inflammatory effects of an ethanol extract of the rhizome of E. bulbosa (EBE) on lipopolysaccharide-stimulated RAW 264.7 macrophages in vitro and in a collagen antibody-induced arthritic (CAIA) mouse model in vivo. Treatment of the CAIA mice with EBE decreased the incidence of arthritis, especially at a dose of 1000 mg/kg body weight. A significant ( P<0.05) decrease in the arthritis score was seen after high-dose EBE treatment between days 10 and 14 in comparison with the negative control. The serum levels of the inflammatory cytokines tumor necrosis factor alpha (TNF-α), interleukin (IL)-6, and IL-10 in the mice were measured using commercial ELISA kits. The results suggest that an ethanol extract of the E. bulbosa rhizome has beneficial effects on inflammatory cytokine regulation in an experimental CAIA model.

scholarly journals Annexin A1 attenuates neutrophil migration and IL-6 expression through Fpr2 in a mouse model of Streptococcus suis-induced meningitis

2020 ◽  
pp. IAI.00680-20
Author(s):  
Chengpei Ni ◽  
Song Gao ◽  
Yuling Zheng ◽  
Peng Liu ◽  
Yajie Zhai ◽  
...  
Keyword(s):  
Mouse Model ◽  
Inflammatory Mediator ◽  
Therapeutic Option ◽  
Neutrophil Migration ◽  
Streptococcus Suis ◽  
Formyl Peptide Receptor ◽  
Annexin A1 ◽  
Formyl Peptide ◽  
Anti Inflammatory

Streptococcus suis (S. suis) serotype 2 is a crucial pathogenic cause of bacterial meningitis, a life-threatening disease with neurological sequelae and high rates of mortality. Inflammation triggered by S. suis infection must be precisely regulated to prevent further tissue damage. As a glucocorticoid anti-inflammatory mediator, Annexin A1 (AnxA1) mainly acts through formyl peptide receptor 2 (Fpr2) to alleviate inflammation in the peripheral system. In this research, we evaluated the roles of AnxA1 and Fpr2 in a mouse model of S. suis meningitis created via intracisternal infection in Fpr2-deficient (Fpr2−/−) and wild-type (WT) mice. We revealed that Fpr2−/− mice were highly susceptible to S. suis meningitis, displaying increased inflammatory cytokine levels, bacterial dissemination, and neutrophil migration compared with the findings in WT mice. Additionally, AnxA1 exerted anti-inflammatory effects through Fpr2, such as attenuation of leukocyte infiltration, inflammatory mediator production, and astrocyte or microglial activation in the brain. Importantly, we found that the anti-migratory function of AnxA1 decreases neutrophil adherence to the endothelium through Fpr2. Finally, an in vitro study revealed that AnxA1 potentially suppresses IL-6 expression through the Fpr2/p38/COX-2 pathway. These data demonstrated that Fpr2 is an anti-inflammatory receptor that regulates neutrophil migration in mice with S. suis meningitis and identified AnxA1 as a potential therapeutic option.

scholarly journals Annexin A1 protects against cerebral ischemia–reperfusion injury by modulating microglia/macrophage polarization via FPR2/ALX-dependent AMPK-mTOR pathway

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Xin Xu ◽  
Weiwei Gao ◽  
Lei Li ◽  
Jiheng Hao ◽  
Bin Yang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Mouse Model ◽  
Clinical Outcomes ◽  
Ischemia Reperfusion ◽  
Macrophage Polarization ◽  
Mtor Pathway ◽  
Annexin A1 ◽  
Cerebral Ischemia Reperfusion ◽  
Anti Inflammatory

Abstract Background Cerebral ischemia–reperfusion (I/R) injury is a major cause of early complications and unfavorable outcomes after endovascular thrombectomy (EVT) therapy in patients with acute ischemic stroke (AIS). Recent studies indicate that modulating microglia/macrophage polarization and subsequent inflammatory response may be a potential adjunct therapy to recanalization. Annexin A1 (ANXA1) exerts potent anti-inflammatory and pro-resolving properties in models of cerebral I/R injury. However, whether ANXA1 modulates post-I/R-induced microglia/macrophage polarization has not yet been fully elucidated. Methods We retrospectively collected blood samples from AIS patients who underwent successful recanalization by EVT and analyzed ANXA1 levels longitudinally before and after EVT and correlation between ANXA1 levels and 3-month clinical outcomes. We also established a C57BL/6J mouse model of transient middle cerebral artery occlusion/reperfusion (tMCAO/R) and an in vitro model of oxygen–glucose deprivation and reoxygenation (OGD/R) in BV2 microglia and HT22 neurons to explore the role of Ac2-26, a pharmacophore N-terminal peptide of ANXA1, in regulating the I/R-induced microglia/macrophage activation and polarization. Results The baseline levels of ANXA1 pre-EVT were significantly lower in 23 AIS patients, as compared with those of healthy controls. They were significantly increased to the levels found in controls 2–3 days post-EVT. The increased post-EVT levels of ANXA1 were positively correlated with 3-month clinical outcomes. In the mouse model, we then found that Ac2-26 administered at the start of reperfusion shifted microglia/macrophage polarization toward anti-inflammatory M2-phenotype in ischemic penumbra, thus alleviating blood–brain barrier leakage and neuronal apoptosis and improving outcomes at 3 days post-tMCAO/R. The protection was abrogated when mice received Ac2-26 together with WRW4, which is a specific antagonist of formyl peptide receptor type 2/lipoxin A4 receptor (FPR2/ALX). Furthermore, the interaction between Ac2-26 and FPR2/ALX receptor activated the 5’ adenosine monophosphate-activated protein kinase (AMPK) and inhibited the downstream mammalian target of rapamycin (mTOR). These in vivo findings were validated through in vitro experiments. Conclusions Ac2-26 modulates microglial/macrophage polarization and alleviates subsequent cerebral inflammation by regulating the FPR2/ALX-dependent AMPK-mTOR pathway. It may be investigated as an adjunct strategy for clinical prevention and treatment of cerebral I/R injury after recanalization. Plasma ANXA1 may be a potential biomarker for outcomes of AIS patients receiving EVT.

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