Abstract
Methylglyoxal (MG) is the primary precursor of advanced glycation end products involved in the pathogenesis of inflammation and diabetes. A previous study in our laboratory found anti-inflammatory and anti-hyperglycemic effects of the polyphenol vescalagin (VES) in rats with MG-induced carbohydrate metabolic disorder. The present study further investigated the occurrence of inflammation in pancreatic β-cells in MG-induced diabetic rats and the mechanism by which VES prevents it. The results showed that VES downregulates the protein expression levels of advanced glycation end product receptors and CCAAT/enhancer binding protein-β and upregulates the protein expression levels of pancreatic duodenal homeobox-1, nuclear factor erythroid 2-related factor 2 and glyoxalase I from the pancreatic cells. The results also revealed that VES elevates glutathione and antioxidant enzyme contents and then downregulates c-Jun N-terminal kinase and p38 mitogen-activated protein kinases pathways to protect pancreatic β-cells in MG-administered rats.
Highlights
Methylglyoxal (MG) is the primary precursor of advanced glycation end products involved in the pathogenesis of inflammation and diabetes
The rats administered orally once a day with MG at 300 mg/kg followed with another chemical (PIO, AG, or VES) at 30 mg/kg for a period of 8 weeks showed no significant difference in diet intake, drink intake, or body weight as compared with the normal group (Table 1), indicating no occurrence of acute-phase response in rats in the feeding period
Results are from 8 repetitions and expressed as mean ± SD
Summary
Methylglyoxal (MG) is the primary precursor of advanced glycation end products involved in the pathogenesis of inflammation and diabetes. MG has been found from animal studies to cause inflammation in Sprague–Dawley rats, to induce their pancreatic impairment, and to affect insulin secretion as a consequence [5]. It appears that the protection of pancreatic β-cells can be an effective way for the maintenance of insulin secretion and the prevention of DM. AGEs may activate advanced glycation end product receptors (RAGE) on the membrane of pancreatic cells and upregulate the two key inflammatory transcription factors, namely early growth response-1 and nuclear factor kappa B (NF-κB) [4,7].
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