Alliin, a garlic (Allium sativum) compound, prevents LPS-induced inflammation in 3T3-L1 adipocytes.
Garlic (Allium sativum L.) 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.
Laboratorio de Desarrollo y Regeneración Neural, Instituto de Neurobiología, Departamento de Biología Celular y Molecular, CUCBA, Universidad de Guadalajara, Camino Ing. R. Padilla Sánchez 2100, Las Agujas, 44600 Zapopan, JAL, Mexico ; Departamento de Farmacobiología, CUCEI, Universidad de Guadalajara, Boulevard Marcelino García Barragán, No. 1421, Esquina Calzada Olímpica, 44430 Guadalajara, JAL, Mexico.
Saray
S
Quintero-Fabián
Laboratorio de Desarrollo y Regeneración Neural, Instituto de Neurobiología, Departamento de Biología Celular y Molecular, CUCBA, Universidad de Guadalajara, Camino Ing. R. Padilla Sánchez 2100, Las Agujas, 44600 Zapopan, JAL, Mexico.
Daniel
D
Ortuño-Sahagún
Unidad de Farmacología, Departamento de Farmacología y Química Terapéutica, Facultad de Farmacia, Institut de Biomedicina de la UB (IBUB) and CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM)-Instituto de Salud Carlos III, 08028 Barcelona, Spain.
Manuel
M
Vázquez-Carrera
Departamento de Farmacobiología, CUCEI, Universidad de Guadalajara, Boulevard Marcelino García Barragán, No. 1421, Esquina Calzada Olímpica, 44430 Guadalajara, JAL, Mexico.
Rocío Ivette
RI
López-Roa
D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000502:physiology; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D018932:Chemokine CCL2 / Q000032:analysis / Q000037:antagonists & inhibitors / Q000235:genetics; D003545:Cysteine / Q000031:analogs & derivatives* / Q000494:pharmacology; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D015850:Interleukin-6 / Q000032:analysis / Q000235:genetics; D008070:Lipopolysaccharides / Q000494:pharmacology*; D051379:Mice; D016328:NF-kappa B / Q000502:physiology; D010766:Phosphorylation; D059467:Transcriptome; D000093242:Interleukin-6 Inhibitors
D000893:Anti-Inflammatory Agents; D018932:Chemokine CCL2; D003545:Cysteine; D048049:Extracellular Signal-Regulated MAP Kinases; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016328:NF-kappa B; D000093242:Interleukin-6 Inhibitors; C491768:Ccl2 protein, mouse; C006453:alliin