Morroniside and loganin extracted from Cornus officinalis have protective effects on rat mesangial cell proliferation exposed to advanced glycation end products by preventing oxidative stress

2006 ◽  
Vol 84 (12) ◽  
pp. 1267-1273 ◽  
Author(s):  
Huiqin Xu ◽  
Jian Shen ◽  
Hong Liu ◽  
Yan Shi ◽  
Lihua Li ◽  
...  

Advanced glycation end products (AGE) are involved in the alterations of renal mesangial cell (MCs) growth, a feature of early stages of diabetic nephropathy (DN). We postulate that morroniside and loganin, 2 components extracted from Cornus officinalis , may ameliorate the detrimental effects of AGE-induced MCs proliferation by preventing oxidative stress. Rat MCs cultured in AGE milieu were treated with morroniside and loganin. Results showed that morroniside and loganin inhibited AGE-induced MC proliferation as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) method. Fluorescence microscopy revealed that the morroniside and loganin improved the morphological changes of MCs. Flow cytometric analysis showed that morroniside and loganin inhibited the cell cycle of rat MCs. Furthermore, the level of reactive oxygen species was significantly reduced, and the activities of superoxide dismutase and glutathione peroxidase were markedly increased, whereas the level of malondialdehyde was not significantly reduced. These results suggest that morroniside and loganin regulate MC growth by preventing oxidative stress. Thus, this study provides a molecular basis for the use of morroniside and loganin in the early stages of DN.

2021 ◽  
Author(s):  
Akio Nakamura ◽  
Ritsuko Kawahrada

Protein glycation is the random, nonenzymatic reaction of sugar and protein induced by diabetes and ageing; this process is quite different from glycosylation mediated by the enzymatic reactions catalysed by glycosyltransferases. Schiff bases form advanced glycation end products (AGEs) via intermediates, such as Amadori compounds. Although these AGEs form various molecular species, only a few of their structures have been determined. AGEs bind to different AGE receptors on the cell membrane and transmit signals to the cell. Signal transduction via the receptor of AGEs produces reactive oxygen species in cells, and oxidative stress is responsible for the onset of diabetic complications. This chapter introduces the molecular mechanisms of disease onset due to oxidative stress, including reactive oxygen species, caused by AGEs generated by protein glycation in a hyperglycaemic environment.


2010 ◽  
Vol 58 (20) ◽  
pp. 11119-11129 ◽  
Author(s):  
Deena Ramful ◽  
Evelyne Tarnus ◽  
Philippe Rondeau ◽  
Christine Robert Da Silva ◽  
Theeshan Bahorun ◽  
...  

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