scholarly journals Yiqi Huoxue Recipe Regulates Autophagy through Degradation of Advanced Glycation End Products via mTOR/S6K1/LC3 Pathway in Diabetic Nephropathy

2021 ◽  
Vol 2021 ◽  
pp. 1-12
Author(s):  
Liang Chen ◽  
Linghao Dai ◽  
Yi Liu ◽  
Xinyue Li ◽  
Hui Wang
Keyword(s):  
Body Weight ◽  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Periodic Acid ◽  
The Body ◽  
Advanced Glycation ◽  
Kidney Weight ◽  
Expression Levels ◽  
Glycation End Products ◽  
End Products

Background. Yiqi Huoxue recipe can delay the progression of diabetic nephropathy, but its treatment mechanism is still unclear. We aimed to explore the effects of Yiqi Huoxue recipe on autophagy in diabetic nephropathy and its underlying mechanism. Methods. All rats were randomly divided into seven groups. The body weight, kidney weight, blood glucose, glycated hemoglobin, urine protein, urine microprotein, creatinine, urea nitrogen, triglyceride, and lipoprotein were analyzed. HE, Masson, and periodic acid-Schiff staining were used to detect the severity of pathological changes in kidneys. The level of advanced glycation end products was assessed by the ELISA. Immunofluorescence staining was performed to check the expressions of podocin and nephrin. The expression levels of mTOR/S6K1/LC3 pathway-related proteins and mRNA were detected by qRT-PCR and western blotting. Results. Yiqi Huoxue recipe significantly elevated body weight and significantly decreased kidney weight and kidney index. Yiqi Huoxue recipe significantly affected the levels of biochemical indicators in diabetic nephropathy and showed a regulatory effect on kidney damage and lipid metabolism disorders. ELISA showed that Yiqi Huoxue recipe significantly reduced the level of advanced glycation end products. The expressions of nephrin and podocin increased significantly, depending on the dosage of Yiqi Huoxue recipe. Additionally, Yiqi Huoxue recipe regulated the expression levels of p-AKT, mTOR, S6K1, and LC3. Conclusion. Yiqi Huoxue recipe regulates podocyte autophagy to promote the degradation of advanced glycation end products through mTOR/S6K1/LC3 pathway. It has a certain guiding significance for the diagnosis and treatment of diabetic nephropathy.

scholarly journals Endogenous Secretory Receptor for Advanced Glycation End Products Protects Endothelial Cells from AGEs Induced Apoptosis

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Guomin Yang ◽  
Yinqiong Huang ◽  
Xiaohong Wu ◽  
Xiahong Lin ◽  
Jinting Xu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Advanced Glycation End Products ◽  
Proinflammatory Cytokine ◽  
Enzyme Linked Immunosorbent Assay ◽  
Advanced Glycation ◽  
Expression Levels ◽  
Qrt Pcr ◽  
Glycation End Products ◽  
End Products

Endogenous secretory receptor for advanced glycation end products (esRAGE) binds extracellular RAGE ligands and blocks RAGE activation on the cell surface, protecting endothelial cell function. However, the underlying mechanism remains unclear. Endothelial cells overexpressing the esRAGE gene were generated using a lentiviral vector. Then, quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) were used to assess esRAGE mRNA and protein levels, respectively. Hoechst-PI double staining was used to assess apoptosis. Western blot and qRT-PCR were used to assess the expression levels of apoptosis-related factors and the proinflammatory cytokine NF-кB. Compared with the control group, AGEs significantly induced endothelial cell apoptosis, which was significantly reduced by esRAGE overexpression. Incubation with AGEs upregulated the proapoptotic factor Bax and downregulated the antiapoptotic factor Bcl-2. Overexpression of esRAGE reduced Bax expression induced by AGEs and increased Bcl-2 levels. Furthermore, AGEs increased the expression levels of proinflammatory cytokine NF-кB, which were reduced after esRAGE overexpression. esRAGE protects endothelial cells from AGEs associated apoptosis, by downregulating proapoptotic (Bax) and inflammatory (NF-кB) factors and upregulating the antiapoptotic factor Bcl-2.

Effect of pyridoxamine (K-163), an inhibitor of advanced glycation end products, on type 2 diabetic nephropathy in KK-Ay/Ta mice

Metabolism ◽  
2007 ◽  
Vol 56 (2) ◽  
pp. 160-167 ◽  
Author(s):  
Mitsuo Tanimoto ◽  
Tomohito Gohda ◽  
Shigeru Kaneko ◽  
Shinji Hagiwara ◽  
Maki Murakoshi ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Type 2 Diabetic

scholarly journals Advanced glycation end-products in diabetic nephropathy

1996 ◽  
Vol 11 (supp5) ◽  
pp. 91-94 ◽  
Author(s):  
S. Sugiyama ◽  
T. Miyata ◽  
K. Horie ◽  
Y. Iida ◽  
M. Tsuyuki ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

AGE, RAGE and Diabetic Nephropathy

2010 ◽  
Vol 8 (2) ◽  
pp. 84
Author(s):  
MaÏté Daroux ◽  
Nicolas Grossin ◽  
Eric Boulanger ◽  
◽  
◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Diabetic Nephropathy ◽  
Kidney Disease ◽  
Advanced Glycation End Products ◽  
Specific Treatment ◽  
Therapeutic Approaches ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Immunohistochemical Studies

Diabetes is a disease that is present worldwide and which is associated with a large number of potential complications including chronic kidney disease (CKD). Several factors have been implicated in the development of the latter, including advanced glycation end-products (AGEs), which are formed from the interaction between sugar and proteins. AGE toxicity may be triggered via different mechanisms, especially by receptor binding. Immunohistochemical studies have demonstrated the presence of AGEs in all renal structures (vessels, glomeruli, tubules and the interstitium). They appear to be involved in the exacerbation of renal injury observed during diabetic nephropathy. At present, no specific treatment is yet available, although several therapeutic approaches are under development.

scholarly journals Roles of advanced glycation end-products in the progression of diabetic nephropathy

1996 ◽  
Vol 11 (supp5) ◽  
pp. 76-80 ◽  
Author(s):  
H. Makino ◽  
K. Shikata ◽  
M. Kushiro ◽  
K. Hironaka ◽  
Y. Yamasaki ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

Ellagic acid inhibits non-enzymatic glycation and prevents proteinuria in diabetic rats

2016 ◽  
Vol 7 (3) ◽  
pp. 1574-1583 ◽  
Author(s):  
G. Raghu ◽  
Sneha Jakhotia ◽  
P. Yadagiri Reddy ◽  
P. Anil Kumar ◽  
G. Bhanuprakash Reddy
Keyword(s):  
Diabetic Nephropathy ◽  
Characteristic Feature ◽  
Advanced Glycation End Products ◽  
Ellagic Acid ◽  
Diabetic Rats ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

The formation of advanced glycation end products (AGEs) is a characteristic feature of diabetic tissues and accumulation of AGEs been implicated in the pathogenesis of diabetic nephropathy (DN). Ellagic acid prevented the accumulation of AGEs and in turn ameliorated proteinurea in diabetic rats.

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