Polyphenols Attenuate Highly-Glycosylated Haemoglobin-Induced Damage in Human Peritoneal Mesothelial Cells.
Carolina Sánchez-RodríguezConcepción PeiróLeocadio Rodríguez-MañasJulián NevadoPublished in: Antioxidants (Basel, Switzerland) (2020)
We investigated the cytoprotective role of the dietary polyphenols on putative damage induced by Amadori adducts in Human Peritoneal Mesothelial Cells (HPMCs). Increased accumulation of early products of non-enzymatic protein glycation-Amadori adducts-in the peritoneal dialysis fluid due to their high glucose, induces severe damage in mesothelial cells during peritoneal dialysis. Dietary polyphenols reportedly have numerous health benefits in various diseases and have been used as an efficient antioxidant in the context of several oxidative stress-related pathologies. HPMCs isolated from different patients were exposed to Amadori adducts (highly glycated haemoglobin, at physiological concentrations), and subsequently treated with several polyphenols, mostly presented in our Mediterranean diet. We studied several Amadori-induced effects in pro-apoptotic and oxidative stress markers, as well as the expression of several pro-inflammatory genes (nuclear factor-kappaB, NF-kB; inducible Nitric Oxide synthetase, iNOS), different caspase-activities, level of P53 protein or production of different reactive oxygen species in the presence of different polyphenols. In fact, cytoprotective agents such as dietary polyphenols may represent an alternate approach to protect mesothelial cells from the cytotoxicity of Amadori adducts. The interference with the Amadori adducts-triggered mechanisms could represent a therapeutic tool to reduce complications associated with peritoneal dialysis in the peritoneum, helping to maintain peritoneal membrane function longer in patients undergoing peritoneal dialysis.
Keyphrases
- peritoneal dialysis
- end stage renal disease
- high glucose
- oxidative stress
- endothelial cells
- induced apoptosis
- diabetic rats
- chronic kidney disease
- nuclear factor
- cell cycle arrest
- signaling pathway
- endoplasmic reticulum stress
- nitric oxide
- patients undergoing
- cell death
- reactive oxygen species
- dna damage
- healthcare
- public health
- toll like receptor
- poor prognosis
- mental health
- induced pluripotent stem cells
- binding protein
- ejection fraction
- hydrogen peroxide
- newly diagnosed
- small molecule
- dna methylation
- anti inflammatory
- gene expression
- prognostic factors
- genome wide
- heat shock