Sulforaphane inhibits advanced glycation end product–induced pericyte damage by reducing expression of receptor for advanced glycation end products

In Chinese medicine, Xiexin decoction (XXD) has been used for the clinical treatment of diabetes for at least 1700 years. The present study was conducted to investigate the effective ingredients of XXD and their molecular mechanisms of antidiabetic nephropathy in rats. Rats with diabetes induced by high-fat diet and streptozotocin were treated with XXD extract for 12 weeks. XXD significantly improved the glucolipid metabolism disorder, attenuated albuminuria and renal pathological changes, reduced renal advanced glycation end-products, inhibited receptor for advanced glycation end-product and inflammation factors expression, suppressed renal nuclear factor-κB pathway activity, and downregulated renal transforming growth factor-β1. The concentrations of multiple components in plasma from XXD were determined by liquid chromatography and tandem mass spectrometry. Pharmacokinetic/pharmacodynamic analysis using partial least square regression revealed that 8 ingredients of XXD were responsible for renal protective effects via actions on multiple molecular targets. Our study suggests that the renal protective role of XXD with multiple effective ingredients involves inhibition of inflammation through downregulation of the nuclear factor-κB pathway, reducing renal advanced glycation end-products and receptor for advanced glycation end-product in diabetic rats.

Download Full-text

A comparative study of sulphated polysaccharide effects on advanced glycation end-product uptake and scavenger receptor class A level in macrophages

Diabetes and Vascular Disease Research ◽

10.1177/1479164119896975 ◽

2020 ◽

Vol 17 (1) ◽

pp. 147916411989697 ◽

Cited By ~ 2

Author(s):

Takashi Nishinaka ◽

Shuji Mori ◽

Yui Yamazaki ◽

Atsuko Niwa ◽

Hidenori Wake ◽

...

Keyword(s):

Advanced Glycation End Products ◽

Chondroitin Sulphate ◽

Scavenger Receptor ◽

Dextran Sulphate ◽

Advanced Glycation ◽

Sulphated Polysaccharides ◽

Advanced Glycation End Product ◽

Class A ◽

Glycation End Products ◽

End Products

Advanced glycation end-products, especially toxic advanced glycation end-products derived from glyceraldehyde (advanced glycation end-product-2) and glycolaldehyde (advanced glycation end-product-3), are biologically reactive compounds associated with diabetic complications. We previously demonstrated that toxic advanced glycation end-products were internalised into macrophage-like RAW264.7 cells through scavenger receptor-1 class A (CD204). Toxic advanced glycation end-product uptake was inhibited by fucoidan, a sulphated polysaccharide and antagonistic ligand for scavenger receptors, suggesting that sulphated polysaccharides are emerging candidates for treatment of advanced glycation end-product–related diseases. In this study, we compared the effects of six types of sulphated and non-sulphated polysaccharides on toxic advanced glycation end-product uptake in RAW264.7 cells. Fucoidan, carrageenan and dextran sulphate attenuated toxic advanced glycation end-product uptake. Fucoidan and carrageenan inhibited advanced glycation end-product-2–induced upregulation of SR-A, while advanced glycation end-product-3–induced upregulation of scavenger receptor-1 class A was only suppressed by fucoidan. Dextran sulphate did not affect scavenger receptor-1 class A levels in toxic advanced glycation end-product–treated cells. Chondroitin sulphate, heparin and hyaluronic acid failed to attenuate toxic advanced glycation end-product uptake. Heparin and hyaluronic acid had no effect on scavenger receptor-1 class A levels, while chondroitin sulphate inhibited advanced glycation end-product-3–induced upregulation of scavenger receptor-1 class A. Taken together, fucoidan and carrageenan, but not the other sulphated polysaccharides examined, had inhibitory activities on toxic advanced glycation end-product uptake and toxic advanced glycation end-product–induced upregulation of scavenger receptor-1 class A, possibly because of structural differences among sulphated polysaccharides.

Download Full-text

Skin advanced glycation end-products evaluation in infants according to the type of feeding and mother’s smoking habits

SAGE Open Medicine ◽

10.1177/2050312116682126 ◽

2016 ◽

Vol 4 ◽

pp. 205031211668212 ◽

Cited By ~ 2

Author(s):

Giovanni Federico ◽

Martina Gori ◽

Emioli Randazzo ◽

Francesco Vierucci

Keyword(s):

Breast Milk ◽

Advanced Glycation End Products ◽

Fetal Development ◽

Advanced Glycation ◽

Smoking During Pregnancy ◽

Advanced Glycation End Product ◽

Breastfed Infants ◽

Glycation End Products ◽

End Products ◽

Pregnancy And Lactation

Objectives: This study was conducted to assess whether formula-fed infants had increased skin advanced glycation end-products compared with breastfed ones. We also evaluated the effect of maternal smoke during pregnancy and lactation on infant skin advanced glycation end-products accumulation. Methods: Advanced glycation end-product–linked skin autofluorescence was measured in 101 infants. Results: In infants born from non-smoking mothers, advanced glycation end-products were higher in formula-fed subjects than in breastfed subjects (0.80 (0.65–0.90) vs 1.00 (0.85–1.05), p < 0.001). Advanced glycation end-products in breastfed infants from smoking mothers were higher than in those from non-smoking mothers (0.80 (0.65–0.90) vs 1.00 (0.90–1.17), p = 0.009). Conclusion: Formula-fed infants had increased amounts of advanced glycation end-products compared with the breastfed ones, confirming that breast milk represents the best food for infants. Breastfed infants from mothers smoking during pregnancy and lactation had increased skin advanced glycation end-products, suggesting that smoke-related advanced glycation end-products transfer throughout breast milk. Moreover, advanced glycation end-products may already increase during gestation, possibly affecting fetal development. Thus, we reinforced that smoking must be stopped during pregnancy and lactation.

Download Full-text