RESEARCH ARTICLE |
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Year : 2013 | Volume
: 45
| Issue : 6 | Page : 556-562 |
The effect of chinese medicine pu-ren-dan on pancreatic angiogenesis in high fat diet/streptozotocin-induced diabetic rats
Binan Lu, Yongfei Bai, Ziliang Du, Shu Chen, D Deligema, Zongran Pang
Institute of Chinese Minority Traditional Medicine, Minzu University of China, Beijing 100081, China
Correspondence Address:
Zongran Pang Institute of Chinese Minority Traditional Medicine, Minzu University of China, Beijing 100081 China
 Source of Support: This work was partly supported by Beijing Natural Science Foundation (NO. 7122091) and Independent Research Project of Minzu University of China (NO. 112KYXJ09), and also supported in part by Academic Scholarship for Doctoral Candidates of Ministry of Education., Conflict of Interest: None  | Check |
DOI: 10.4103/0253-7613.121364
Objectives: The islet vascular system is critical for β-cell function. This study investigated the antidiabetic effect of the Chinese Pu-Ren-Dan (PRD) recipe by regulating the pancreatic angiogenic factors in T2DM rats.
Materials Methods: High fat diet/streptozotocin-induced obese type-2 diabetes mellitus rats were developed and treated with PRD for 4 weeks. Then glucolipid metabolism, insulin secretion, pancreatic blood flow, ultrastructure of islet β-cell, histological changes of islet and protein expressions of pancreatic angiogenic factors were investigated.
Results: PRD-reduced T2DM rats' body weight and blood glucose level resisted the lipid metabolism disturbance, and ameliorated the insulin resistance and β-cell function. In addition, the histological and morphological studies proved that PRD could maintain the normal distribution of endocrine cell in islet and normal ultrastructure of β cell. An increased pancreatic blood flow was observed after the PRD treatment. In the investigation of pancreatic angiogenic factors, PRD inhibited the decreased expression of VEGF and Ang-1, and reversed the reduction of VEGFR2 and Tie2 phosphorylation in T2DM rats; the Ang-2 and TGFβ expression were up-regulated by PRD while PKC was activated; endostatin and angiostatin were down-regulated by PRD.
Conclusions: The results suggest that increasing VEGF expression, regulating VEGF/VEGFR2 signaling, stimulating Ang-1/Tie-2 signaling pathway, and inhibiting PKC-TGFβ signaling and antiangiogenic factors might be the underlying mechanism of PRD's antidiabetic effect.
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