β-N-Oxalyl-L-α,β-diaminopropionic acid from Panax notoginseng plays a major role in the treatment of type 2 diabetic nephropathy - 17/05/19
, Junsheng Wu b, Qiaoyan He a, Kaifeng Li a, Lu Xu aBienvenue sur EM-consulte, la référence des professionnels de santé.
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Graphical abstract |
The flowchart to show the effect of Dencichine from Panax notoginseng on STZ-induced nephrotoxicity. Firstly, the ten most highly concentrated components of Panax notoginseng were screened in vitro. Secondly, The STZ-induced DN rat model on a high-fat-high-glucose diet was used to investigate the renal protective effect of Panax notoginseng and Dencichine. Finally, their underlying molecular mechanisms were investigated by immunology and molecular biology methods. As a result, glycolipid metabolism and renal function were improved, kidney damage was relieved by reducing collagen and glycogen deposition, and collagen deposition and epithelial-mesenchymal transformation were inhibited through inhibiting the TGF-β/Smad signaling pathway.
Highlights |
• | We studied the anti-diabetic nephropathy properties of Panax notoginseng in vitro and in vivo after screening its ten main components. We found that Panax notoginseng inhibited high glucose induced mesangial cell proliferation and collagen secretion. |
• | Dencichine can significantly improve disorders of glucose and lipid metabolism in diabetic nephropathy (DN), improve renal function, and significantly improve renal injury caused by type 2 diabetes mellitus. |
• | Dencichine can delay the progression of diabetic nephropathy to renal fibrosis by reducing the accumulation of the extracellular matrix, inhibiting the proliferation of mesangial cells, and inhibiting the transformation of renal epithelial mesenchymal cells. |
• | Dencichine can significantly inhibit the expression of TGF-β and Smad 2 in the TGF-β1/Smad signalling pathway, and up-regulate the expression of Smad7, an endogenous inhibitor. It is suggested that the mechanism by which dencichine improves renal injury in diabetic nephropathy may be related to the inhibition of the TGF-β1/Smad signalling pathway. |
Abstract |
Background |
Diabetic nephropathy (DN) is one of the most serious and dangerous chronic complications of diabetes mellitus.Panax notoginseng has been widely used with great efficacy in the long-term treatment of kidney disease. However, the mechanism by which it exerts its effects has not been fully elucidated.
Aim |
We sought to identify the major components ofPanax notoginseng that are effective in reducing the symptoms of DN in vitro and in vivo.
Methods |
Inhibition of cell proliferation and collagen secretion were used to screen the ten most highly concentrated components ofPanax notoginseng. The STZ-induced DN rat model on a high-fat-high-glucose diet was used to investigate the renal protective effect of Panax notoginseng and dencichine and their underlying molecular mechanisms.
Results |
Among the ten components analysed, dencichine (β-N-oxalyl-L-α,β-diaminopropionic acid) was the most protective against DN. Dencichine andPanax notoginseng attenuated glucose and lipid metabolic disorders in STZ-induced DN rats on a high-fat-high-glucose diet. In the untreated DN rats, we observed albuminuria, renal failure, and pathological changes. However, treatment with dencichine and Panax notoginseng alleviated these symptoms. We also observed that dencichine suppressed the expression of TGF-β1 and Smad2/3, which mediates mesangial cell proliferation and extracellular matrix (ECM) accumulation in the glomerulus, and enhanced the expression of Smad7, the endogenous inhibitor of the TGF-β1/Smad signalling pathway.
Conclusion |
From these results, we concluded that dencichine is the main compound inPanax notoginseng that is responsible for alleviating renal injury in the experimental DN model. Its mechanism may be related to the reduction of the deposition of ECM in glomeruli and inhibition of the epithelial mesenchymal transformation (EMT) by inhibition of the TGF-β1/Smad signalling pathway.
Le texte complet de cet article est disponible en PDF.Abbreviations : BUN, HDL, Col-I, LDL, Col-IV, LN, De, MMP-9, DM, NG, DN, TCH, ECM, TG, FN, TGF-β1, HbAlc, TIMP-1
Keywords : Diabetic nephropathy, Dencichine, β-N-oxalyl-L-α,β-diaminopropionic acid, Panax notoginseng, Extracellular matrix, TGF-β1/Smad signalling pathway
Plan
Vol 114
Article 108801- juin 2019 Retour au numéro
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