scholarly journals Alliin, a Garlic (Allium sativum) Compound, Prevents LPS-Induced Inflammation in 3T3-L1 Adipocytes

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Saray Quintero-Fabián ◽  
Daniel Ortuño-Sahagún ◽  
Manuel Vázquez-Carrera ◽  
Rocío Ivette López-Roa
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Allium Sativum ◽  
Serum Levels ◽  
Organosulfur Compounds ◽  
Inflammatory Gene Expression ◽  
Cytokine Levels ◽  
Anti Inflammatory ◽  
Neuroprotective Actions

Garlic (Allium sativumL.) has been used to alleviate a variety of health problems due to its high content of organosulfur compounds and antioxidant activity. The main active component is alliin (S-allyl cysteine sulfoxide), a potent antioxidant with cardioprotective and neuroprotective actions. In addition, it helps to decrease serum levels of glucose, insulin, triglycerides, and uric acid, as well as insulin resistance, and reduces cytokine levels. However its potential anti-inflammatory effect is unknown. We examined the effects of alliin in lipopolysaccharide- (LPS-) stimulated 3T3-L1 adipocytes by RT-PCR, Western blot, and microarrays analysis of 22,000 genes. Incubation of cells for 24 h with 100 μmol/L alliin prevented the increase in the expression of proinflammatory genes, IL-6, MCP-1, and Egr-1 in 3T3-L1 adipocytes exposed to 100 ng/mL LPS for 1 h. Interestingly, the phosphorylation of ERK1/2, which is involved in LPS-induced inflammation in adipocytes, was decreased following alliin treatment. Furthermore, the gene expression profile by microarrays evidentiate an upregulation of genes involved in immune response and downregulation of genes related with cancer. The present results have shown that alliin is able to suppress the LPS inflammatory signals by generating an anti-inflammatory gene expression profile and by modifying adipocyte metabolic profile.

scholarly journals AS601245, an Anti-Inflammatory JNK Inhibitor, and Clofibrate Have a Synergistic Effect in Inducing Cell Responses and in Affecting the Gene Expression Profile in CaCo-2 Colon Cancer Cells

PPAR Research ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-16 ◽  
Author(s):  
Angelo Cerbone ◽  
Cristina Toaldo ◽  
Stefania Pizzimenti ◽  
Piergiorgio Pettazzoni ◽  
Chiara Dianzani ◽  
...  
Keyword(s):  
Gene Expression ◽  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Combined Treatment ◽  
Colon Cancer Cells ◽  
Positive Interaction ◽  
Anti Inflammatory

PPARαs are nuclear receptors highly expressed in colon cells. They can be activated by the fibrates (clofibrate, ciprofibrate etc.) used to treat hyperlipidemia. Since PPARαtranscriptional activity can be negatively regulated by JNK, the inhibition of JNK activity could increase the effectiveness of PPARαligands. We analysed the effects of AS601245 (a JNK inhibitor) and clofibrate alone or in association, on proliferation, apoptosis, differentiation and the gene expression profile of CaCo-2 human colon cancer cells. Proliferation was inhibited in a dose-dependent way by clofibrate and AS601245. Combined treatment synergistically reduced cell proliferation, cyclin D1 and PCNA expression and induced apoptosis and differentiation. Reduction of cell proliferation, accompanied by the modulation of p21 expression was observed in HepG2 cells, also. Gene expression analysis revealed that some genes were highly modulated by the combined treatment and 28 genes containing PPRE were up-regulated, while clofibrate alone was ineffective. Moreover, STAT3 signalling was strongly reduced by combined treatment. After combined treatment, the binding of PPARαto PPRE increased and paralleled with the expression of the PPAR coactivator MED1. Results demonstrate that combined treatment increases the effectiveness of both compounds and suggest a positive interaction between PPARαligands and anti-inflammatory agents in humans.

scholarly journals A distinct inflammatory gene expression profile in patients with psoriatic arthritis

2006 ◽  
Vol 7 (7) ◽  
pp. 583-591 ◽  
Author(s):  
A K Stoeckman ◽  
E C Baechler ◽  
W A Ortmann ◽  
T W Behrens ◽  
C J Michet ◽  
...  
Keyword(s):  
Gene Expression ◽  
Psoriatic Arthritis ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene

Quercetin-3-O-glucuronide affects the gene expression profile of M1 and M2a human macrophages exhibiting anti-inflammatory effects

2012 ◽  
Vol 3 (11) ◽  
pp. 1144 ◽  
Author(s):  
Eleonora Derlindati ◽  
Margherita Dall'Asta ◽  
Diego Ardigò ◽  
Furio Brighenti ◽  
Ivana Zavaroni ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Human Macrophages ◽  
Anti Inflammatory

scholarly journals Gene Expression Profile of Coronary Artery Cells Treated With Nonsteroidal Anti-inflammatory Drugs Reveals Off-target Effects

2012 ◽  
Vol 59 (6) ◽  
pp. 487-499 ◽  
Author(s):  
Sanjeewani T. Palayoor ◽  
Molykutty J-Aryankalayil ◽  
Adeola Y. Makinde ◽  
David Cerna ◽  
Michael T. Falduto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Coronary Artery ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Inflammatory Drugs ◽  
Anti Inflammatory ◽  
Target Effects

scholarly journals Gene Expression Profiling and Functional Characterization of Macrophages in Response to Circulatory Microparticles Produced during Trypanosoma cruzi Infection and Chagas Disease

2016 ◽  
Vol 9 (2) ◽  
pp. 203-216 ◽  
Author(s):  
Imran H. Chowdhury ◽  
Sue-jie Koo ◽  
Shivali Gupta ◽  
Lisa Yi Liang ◽  
Bojlul Bahar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Trypanosoma Cruzi ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Nitrosative Stress ◽  
Disease State ◽  
Inflammatory Gene Expression ◽  
Inflammatory Gene ◽  
Ifn Γ

Background: Chronic inflammation and oxidative stress are hallmarks of chagasic cardiomyopathy (CCM). In this study, we determined if microparticles (MPs) generated during Trypanosoma cruzi (Tc) infection carry the host's signature of the inflammatory/oxidative state and provide information regarding the progression of clinical disease. Methods: MPs were harvested from supernatants of human peripheral blood mononuclear cells in vitro incubated with Tc (control: LPS treated), plasma of seropositive humans with a clinically asymptomatic (CA) or symptomatic (CS) disease state (vs. normal/healthy [NH] controls), and plasma of mice immunized with a protective vaccine before challenge infection (control: unvaccinated/infected). Macrophages (mφs) were incubated with MPs, and we probed the gene expression profile using the inflammatory signaling cascade and cytokine/chemokine arrays, phenotypic markers of mφ activation by flow cytometry, cytokine profile by means of an ELISA and Bioplex assay, and oxidative/nitrosative stress and mitotoxicity by means of colorimetric and fluorometric assays. Results:Tc- and LPS-induced MPs stimulated proliferation, inflammatory gene expression profile, and nitric oxide (∙NO) release in human THP-1 mφs. LPS-MPs were more immunostimulatory than Tc-MPs. Endothelial cells, T lymphocytes, and mφs were the major source of MPs shed in the plasma of chagasic humans and experimentally infected mice. The CS and CA (vs. NH) MPs elicited >2-fold increase in NO and mitochondrial oxidative stress in THP-1 mφs; however, CS (vs. CA) MPs elicited a more pronounced and disease-state-specific inflammatory gene expression profile (IKBKB, NR3C1, and TIRAP vs. CCR4, EGR2, and CCL3), cytokine release (IL-2 + IFN-γ > GCSF), and surface markers of mφ activation (CD14 and CD16). The circulatory MPs of nonvaccinated/infected mice induced 7.5-fold and 40% increases in ∙NO and IFN-γ production, respectively, while these responses were abolished when RAW264.7 mφs were incubated with circulatory MPs of vaccinated/infected mice. Conclusion: Circulating MPs reflect in vivo levels of an oxidative, nitrosative, and inflammatory state, and have potential utility in evaluating disease severity and the efficacy of vaccines and drug therapies against CCM.

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