Abstract
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.
Highlights
Obesity has been traditionally linked to metabolic dysfunction, led by adipocyte proliferation and hypertrophy [1]
Some studies have shown the relevance of 3T3-L1 adipocytes, fully differentiated in vitro and stimulated by LPS, as a useful model to test for molecules that exhibits an anti-inflammatory effect and that are able to modulate the inflammatory state of adipose tissue [37]
When we analyzed in detail the genes upregulated by alliin pretreatment with a higher median zscore (>2.5) in two comparisons, we found 10 genes related with immunoglobulin production and with T-cell receptors (Table 2), suggesting that alliin could exert an effect on the 3T3-L1 adipocytes inducing lymphopoietic activities
Summary
Obesity has been traditionally linked to metabolic dysfunction, led by adipocyte proliferation and hypertrophy [1]. Some other systemic alterations are being studied as related to obesity, for example, inflammation and immune dysfunction [2]. Adipose tissue is widely considered as an endocrine tissue capable of producing chronic inflammatory responses [3,4,5]. Obesity has been shown to cause an increase in plasma concentrations of a number of proinflammatory markers (e.g., IL-6, TNF-α) that are expressed and released by adipocytes [6]. Diet-induced obesity increases local and systemic inflammatory adipocytokines in humans and in rodents; these factors contribute to adverse health outcomes [7]. Therapies able to modulate the inflammatory state of adipose tissue are being considered for the treatment of obesity [9]. Factors that might mitigate or act against this inflammatory response have remained elusive
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