Fermented Supernatants of Lactobacillus plantarum GKM3 and Bifidobacterium lactis GKK2 Protect against Protein Glycation and Inhibit Glycated Protein Ligation.

With age, protein glycation in organisms increases continuously. Evidence from many studies shows that the accumulation of glycated protein is highly correlated with biological aging and the development of aging-related diseases, so developing a dietary agent to attenuate protein glycation is very meaningful. Previous studies have indicated that lactic acid bacteria-fermented products have diverse biological activities especially in anti-aging, so this study was aimed to investigate the inhibitory effect of the fermented supernatants of Lactobacillus plantarum GKM3 (GKM3) and Bifidobacterium lactis GKK2 (GKK2) on protein glycation. The results show that GKM3- and GKK2-fermented supernatants can significantly inhibit protein glycation by capturing a glycation agent (methylglyoxal) and/or protecting functional groups in protein against methylglyoxal-induced responses. GKM3- and GKK2-fermented supernatants can also significantly inhibit the binding of glycated proteins to the receptor for advanced glycation end products (RAGE). In conclusion, lactic acid bacteria fermentation products have the potential to attenuate biological aging by inhibiting protein glycation.

Naturally occurring flavonoids attenuate high glucose-induced expression of proinflammatory cytokines in human monocytic THP-1 cells.

Activation of circulating monocytes by hyperglycemia is bound to play a role in inflammatory and atherosclerosis. In this study, we examined whether flavonoids (catechin, EGCG, luteolin, quercetin, rutin) - phytochemicals that may possible belong to a new class of advanced glycation end products (AGEs) inhibitors - can attenuate high glucose (15 mmol/L, HG)-induced inflammation in human monocytes. Our results show that all flavonoids significantly inhibited HG-induced expression of proinflammatory genes and proteins, including TNF-alpha, interleukin-1beta (IL-1beta), and cyclooxygenase (COX)-2, at a concentration of 20 microM. Flavonoids also prevented oxidative stress in activated monocytes, as demonstrated by their inhibitory effects on intracellular reactive oxygen species (ROS) and N(epsilon)-(carboxymethyl)lysine formation caused by HG. These inhibitory effects may involve inhibition of nuclear factor-kappaB activation and may be supported by downregulation of the following: i) PKC-dependent NADPH oxidase pathway; ii) phosphorylation of p38 mitogen-activated protein kinase and extracellular signal-regulated protein kinase, and iii) mRNA expression of receptor of AGEs. In addition, we found for the first time that lower levels of Bcl-2 protein under HG conditions could be countered by the action of flavonoids. Our data suggest that, along with their antioxidant activities, flavonoids possess anti-inflammatory properties and might therefore have additional protective effects against glycotoxin-related inflammation.