Effect of Pholiota nameko Polysaccharides Inhibiting Methylglyoxal-Induced Glycation Damage In Vitro.
His LinTing-Yun LinJer-An LinKuan Chen ChengShella Permatasari SantosoChun-Hsu ChouChang-Wei HsiehPublished in: Antioxidants (Basel, Switzerland) (2021)
Advanced glycation end products (AGEs) can induce oxidative stress and inflammation. AGEs are major risk factors for the development of many aging-related diseases, such as cancer and diabetes. In this study, Pholiota nameko polysaccharides (PNPs) were prepared from water extract of P. nameko via graded alcohol precipitation (40%, 60%, and 80% v/v). We explored the in vitro antiglycation ability of the PNPs and inhibition of methylglyoxal (MG)-induced Hs68 cell damage. In a bovine serum albumin (BSA) glycation system, PNPs significantly inhibited the formation of Amadori products. Fluorescence spectrophotometry revealed that the PNPs trapped MG and reduced MG-induced changes in functional groups (carbonyl and ε-NH2) in the BSA. Pretreating Hs68 cells with PNPs enhanced the cell survival rate and protected against MG-induced cell damage. This was due to decreased intracellular ROS content. PNPs thus mitigate skin cell damage and oxidative stress resulting from glycation stress, making them a potential raw material for antiaging-related skincare products.
Keyphrases
- oxidative stress
- diabetic rats
- induced apoptosis
- single cell
- dna damage
- high glucose
- ischemia reperfusion injury
- cell therapy
- drug induced
- cardiovascular disease
- type diabetes
- reactive oxygen species
- signaling pathway
- climate change
- endothelial cells
- endoplasmic reticulum stress
- risk assessment
- papillary thyroid
- soft tissue
- human health
- energy transfer
- heat shock protein
- single molecule