Polydatin, A Natural Precursor of Resveratrol, Induces β-Defensin Production and Reduces Inflammatory Response

Abstract

Abstract-It is well known that human keratinocytes produce the anti-microbial peptide β-defensin 2. Its production is enhanced by pathogenic microorganisms or other environmental stressors. In this study, we evaluated the effect of resveratrol, a polyphenol found in several dietary source as grape seed, and its natural precursor, polydatin on heat-stressed human keratinocytes. By reverse transcription-polymerase chain reaction and enzyme-linked immunoadsorbent assay, we demonstrated that resveratrol used in combination with polydatin was able to modulate interleukin (IL)-6, IL-8 and tumor necrosis factor-alpha gene expression. In addition, our data show that resveratrol and polydatin increased the heat shock protein (Hsp)70B′ gene expression, a Hsp that plays an important role in the cytoprotection and repair of cells and tissues. Worthy of note, polydatin used alone or in combination with resveratrol, increased the release of human β-defensin 2. These results highlighted the ability of polydatin and resveratrol to reinforce cytoprotective response in stress conditions and suggest their use in cosmetic or pharmaceutical preparations.

Basal and stress-inducible expression of HSPA6 in human keratinocytes is regulated by negative and positive promoter regions

“…Consistent with a recent report (GomezSucerquia et al 2012), our studies demonstrate detectable but variable levels of constitutive HSPA6 protein in all human cell types examined. Basal expression of HSPA6 could be dependent on different cell growth conditions, such as cell density (Noonan et al 2007b) or cell culture media (Wu and Morimoto 1985;Zachova et al 2009), and may address the HSPA6 detection here but not in prior analysis of HaCaT keratinocytes (Ravagnan et al 2013). Upon thermal stress, HaCaT keratinocytes responded with induction of both HSPA1A and A6, although the latter to many more fold at the mRNA level.…”

Polydatin: A review of pharmacology and pharmacokinetics

“…PD activates aryl hydrocarbon receptor machinery in UV-exposed keratinocytes through down-regulating the gene expression of pro-inflammatory cytokines/enzymes, suppressing interferon gamma-inducible protein 10 (IP-10) release, and up-regulating IL-8 level (Potapovich et al, 2011), opposing enhanced monocyte chemotactic protein-1 (MCP-1) and IP-10 transcription/synthesis (Pastore et al, 2012). PD is also able to modulate IL-6, IL-8 and TNF-a gene expression, increase the release of human b-defensin 2 and gene expression of heat shock protein 70B 0 in heat-stressed HaCaT (Ravagnan et al, 2013). PD enhances fibroblast proliferation at the concentrations of 10 -5 and 10 À4 mol/L but blocks the cellular cycle in S phase at 10 À3 mol/L, suggesting its bidirectional regulatory effects in fibroblasts .…”

Polydatin post-treatment alleviates myocardial ischaemia/reperfusion injury by promoting autophagic flux

“…The difference between PD (3,4,5-trihydroxystilbene-3-β-mon-D-glucoside) and RES (3,4,5-trihydroxystilbene) is the substitution of a glucoside group at the position C-3 of PD instead of a hydroxy group [4] (Figure 1A). Similar to RES, PD exerts multiple pharmacological effects, such as antioxidant and antiinflammatory activity [4,5], and alleviation of pressure overloadinduced cardiac remodelling [6,7]. Further, PD has more potent antioxidant effects than RES due to its specialized biological properties resulting from the conformational difference from RES [4,8].…”