scholarly journals A Network Pharmacology Approach to Investigate the Mechanism of Erjing Prescription in Type 2 Diabetes

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Jiexin Wang ◽  
Haiqing Chu ◽  
Hangying Li ◽  
Wenqian Yang ◽  
Yu Zhao ◽  
...  

Erjing prescription (EJP) was an ancient formula that was recorded in the General Medical Collection of Royal Benevolence of the Song Dynasty. It has been frequently used to treat type 2 diabetes mellitus (T2DM) in the long history of China. The formula consists of Lycium barbarum L. and Polygonatum sibiricum F. Delaroche with a ratio of 1 : 1. This study aimed to identify the potential effects and mechanisms of EJP treatment T2DM. The target proteins and possible pathways of EJP in T2DM treatment were investigated by the approach of network pharmacology and real-time PCR (RT-PCR). 99 diabetes-related proteins were regulated by 56 bioactive constituents in EJP in 26 signal pathways by Cytoscape determination. According to GO analysis, 606 genes entries have been enriched. The PPI network suggested that AKT1, EGF, EGFR, MAPK1, and GSK3β proteins were core genes. Among the 26 signal pathways, the PI3K-AKT signal pathway was tested by the RT-PCR. The expression level of PI3K p85, AKT1, GSK3β, and Myc mRNA of this pathway was regulated by EJP. The study based on network pharmacology and RT-PCR analysis revealed that the blood sugar level was regulated by EJP via regulating the PI3K-AKT signal pathway. Plenty of new treatment methods for T2DM using EJP were provided by network pharmacology analysis.

2021 ◽  
Author(s):  
Feng Xu ◽  
Hongmei Wu ◽  
Yuanmin Wang ◽  
Ye Yang ◽  
Xiangpei Wang

Abstract Background: Lupenone (LUP) is the active ingredient of Rhizoma Musae, which has good anti-diabetes effects, but the underlying mechanism is unclear. In this study, animal experiments combined with network pharmacology were used to explore the mechanism of LUP for treating diabetes. Methods: Type 2 diabetic rats with insulin resistance (IR) were induced by a high-fat diet and streptozotocin. the fasting blood glucose (FBG), index of oxidative stress, blood lipids, and IR-related targets in skeletal muscle and adipose were detected. a network pharmacology-based strategy was also adopted to clarify the mechanism of LUP for treating diabetes by improving IR. Results: LUP decreased the FBG levels and synthesis of glycogen, improved oxidative stress and lipid metabolism disorders, and increased the gene and protein expression of insulin receptor, insulin receptor substrate (IRS)-1, IRS-2, glucose transporter type 4 (GLUT-4) in skeletal muscle and peroxisome proliferator-activated receptor γ, IRS-1, IRS-2, GLUT-4 in adipose. Network pharmacology analysis revealed that LUP improves IR by multiple targets (like INS, TP53, TNF, SRC and ESR1) and signal pathways. Conclusion: These results suggested that the mechanism of LUP for treating diabetes is closely related to improving IR. LUP has the potential to develop as a new drug for the treatment of type 2 diabetes.


Diabetes Care ◽  
2005 ◽  
Vol 28 (2) ◽  
pp. 379-384 ◽  
Author(s):  
L. Feng ◽  
C. Matsumoto ◽  
A. Schwartz ◽  
A. M. Schmidt ◽  
D. M. Stern ◽  
...  

2021 ◽  
Vol 2021 ◽  
pp. 1-14
Author(s):  
Guozhen Yuan ◽  
Shuai Shi ◽  
Qiulei Jia ◽  
Jingjing Shi ◽  
Shuqing Shi ◽  
...  

Rapid increases in metabolic disorders, such as type 2 diabetes mellitus (T2DM) and hyperlipidemia, are becoming a substantial challenge to worldwide public health. Traditional Chinese medicine has a long history and abundant experience in the treatment of diabetes and hyperlipidemia, and Puerariae lobatae Radix (known as Gegen in Chinese) is one of the most prevalent Chinese herbs applied to treat these diseases. The underlying mechanism by which Gegen simultaneously treats diabetes and hyperlipidemia, however, has not been clearly elucidated to date. Therefore, we systematically explored the potential mechanism of Gegen in the treatment of T2DM complicated with hyperlipidemia based on network pharmacology. We screened the potential targets of Gegen, T2DM, and hyperlipidemia in several online databases. Then, the hub targets were analyzed by performing protein-protein interaction, Gene Ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment assays, and finally, the complicated connections among compounds, targets, and pathways were visualized in Cytoscape. We found that isoflavones, including daidzein, genistein, and puerarin, as well as β-sitosterol, are the key active ingredients of Gegen responsible for its antidiabetic and antihyperlipidemia effects, which mainly target AKR1B1, EGFR, ESR, TNF, NOS3, MAPK3, PPAR, CYP19A1, INS, IL6, and SORD and multiple pathways, such as the PI3K-Akt signaling pathway; the AGE-RAGE signaling pathway in diabetic complications, fluid shear stress, and atherosclerosis; the PPAR signaling pathway; insulin resistance; the HIF-1 signaling pathway; the TNF signaling pathway; and others. These active ingredients also target multiple biological processes, including the regulation of glucose and lipid metabolism, the maintenance of metabolic homeostasis, and anti-inflammatory and antioxidant pathways. In conclusion, Gegen is a promising therapeutic phytomedicine for T2DM with hyperlipidemia that targets multiple proteins, biological processes, and pathways.


2009 ◽  
Vol 55 (5) ◽  
pp. 43-48 ◽  
Author(s):  
V Shvarts

This review deals with the role of adipose tissue inflammation (ATI) in the development of type 2 diabetes mellitus (DM2). ATI is regarded as a link between obesity and DM2. The review illustrates the involvement of main adipokines in pathogenesis of DM2 and provides a detailed description of such factors as impaired adiponectin and stimulation of cytokine production responsible for metabolic disorders, activation of lipolysis, in adipocytes, increased fatty acid and triglyceride levels, suppression of insulin activity at the receptor and intracellular levels. Adipokines, in the first place cytokines, act on the insulin signal pathway and affect the intracellular inflammatory kinase cascade. At the intercellular level, ATI stimulates JNK and IKK-beta/kB responsible for the development of insulin resistance via such mechanisms as activation of cytokine secretion in the adipose tissue, oxidative stress, and induction of endoplasmic reticulum enzymes. The key role of JNK and IKK-beta/kB in the inhibition of the insulin signal pathway is mediated through inactivation of insulin receptor substrate 1. Also, it is shown that ATI modulates B-cell function and promotes progressive reduction of insulin secretion.


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