Inflammatory bowel diseases (IBD) arise from multiple causes, including environmental factors, gut microflora, immunity, and genetic predispositions. In the course of IBD, immune homeostasis and intestinal mucosa barrier integrity are impaired. Among natural preventive treatments that have been identified to date, polyphenols appear as promising candidates. They have been shown to protect against several diseases, including cardiovascular diseases and cancers, and they have anti-inflammatory properties in non-intestinal models. This paper will review the literature that has described to date some effects of polyphenols on intestinal inflammation. Studies, conducted using in vivo and in vitro models, provide evidence that pure polyphenolic compounds and natural polyphenolic plant extracts can modulate intestinal inflammation.

Cardiovascular diseases (CVDs) are the leading cause of death worldwide and represent a major problem of public health. Over the years, life expectancy has considerably increased throughout the world, and the prevalence of CVD is inevitably rising with the growing ageing of the population. The normal process of ageing is associated with progressive deterioration in structure and function of the vasculature, commonly called vascular ageing. At the vascular level, extracellular matrix (ECM) ageing leads to molecular alterations in long half-life proteins, such as elastin and collagen, and have critical effects on vascular diseases. This review highlights ECM alterations occurring during vascular ageing with a specific focus on elastin fragmentation and also the contribution of elastin-derived peptides (EDP) in age-related vascular complications. Moreover, current and new pharmacological strategies aiming at minimizing elastin degradation, EDP generation, and associated biological effects are discussed. These strategies may be of major relevance for preventing and/or delaying vascular ageing and its complications.

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Recent studies support beneficial effects of polyphenols in various chronic inflammatory diseases, for example, the inflammatory bowel diseases. Inhibition of NF-kB activation by polyphenols could explain part of their anti-inflammatory properties, but few data are available on the intestine. The purpose of the present study was thus to investigate the effects of some polyphenols on NF-kB activation using human intestinal Caco-2 cells. Effects of standard polyphenols (50 mmol/l) were studied on different cellular events associated with NF-kB activation: (i) NF-kB activity using cells transiently transfected with a NF-kB -luciferase construct and stimulated by inflammatory agents (IL-1b, TNF-a or lipopolysaccharides (LPS)); (ii) phosphorylation of the inhibitor of kB (IkB-a) analysed by Western blot; (iii) secretion of IL-8 quantified by ELISA assay. Results showed that chrysin and ellagic acid inhibited NF-kB activity, whereas genistein and resveratrol increased it. These effects were independent of the nature of the inducer, indicating that polyphenols may modulate NF-kB activation by acting on a common event to the cytokine-and LPSmediated cascades. Chrysin strongly reduced (2·5-fold) IL-1b-induced IkB-a phosphorylation, whereas ellagic acid increased it (1·7-fold). Ellagic acid, genistein and epigallocatechin gallate reduced (4-to 8-fold) IL-1b-induced IL-8 secretion, while resveratrol promoted (1·7-fold) the secretion. Chrysin also diminished IL-8 secretion by 1·6-fold (but P. 0·05). The data indicate that polyphenols can modulate the NF-kB activation pathway in the intestine. Chrysin could block NF-kB activation via the inhibition of IkB-a phosphorylation. The other molecular targets of the active polyphenols are still to be identified.

Although it has long been established that the extracellular matrix acts as a mechanical support, its degradation products, which mainly accumulate during aging, have also been demonstrated to play an important role in cell physiology and the development of cardiovascular and metabolic diseases. In the current study, we show that elastin-derived peptides (EDPs) may be involved in the development of insulin resistance (IRES) in mice. In chow-fed mice, acute or chronic intravenous injections of EDPs induced hyperglycemic effects associated with glucose uptake reduction and IRES in skeletal muscle, liver, and adipose tissue. Based on in vivo, in vitro, and in silico approaches, we propose that this IRES is due to interaction between the insulin receptor (IR) and the neuraminidase-1 subunit of the elastin receptor complex triggered by EDPs. This interplay was correlated with decreased sialic acid levels on the β-chain of the IR and reduction of IR signaling. In conclusion, this is the first study to demonstrate that EDPs, which mainly accumulate with aging, may be involved in the insidious development of IRES.

The improvement of both proinflammatory status and glucose uptake in adipocytes under 1,25-(OH)(2) D(3) effect suggests that low-grade inflammation could be linked to vitamin D deficiency. This observation offers new perspectives in the context of obesity and associated physiopathological disorders.

Altogether, these data are evidence of a proinflammatory loop mediated by NF-κB and miR-155 that could participate in the amplification of inflammatory status in adipocytes.

These data indicate that lycopene displayed an anti-inflammatory effect on macrophages that beneficially impacted adipocyte function. Thus, these results suggest that lycopene could block the vicious cycle that occurs between adipocytes and macrophages in adipose tissue during obesity.