| Title |
Icariside II ameliorates diabetic nephropathy in streptozotocin-induced diabetic rats
|
|---|---|
| Published in |
Drug Design, Development and Therapy, September 2015
|
| DOI | 10.2147/dddt.s90060 |
| Pubmed ID | |
| Authors |
Wenjie Tian, Hongen Lei, Ruili Guan, Yongde Xu, Huixi Li, Lin Wang, Bicheng Yang, Zhezhu Gao, Zhongcheng Xin |
| Abstract |
To investigate the therapeutic effects and potential mechanisms of icariside II (ICA II) on reversing diabetic nephropathy in streptozotocin (STZ)-induced type I diabetic rats. Newborn male Sprague Dawley rats were labeled with thymidine analog 5-ethynyl-2-deoxyuridine (EdU) for tracking endogenous label retaining progenitor cells (LRCs). At age of 8 weeks, 48 rats were randomly divided into three groups: normal control group (n=16), diabetes mellitus group (DM; n=16), and diabetes mellitus plus ICA II therapy group (DM+ICA II, n=16). Eight weeks induced for diabetes with STZ, rats in DM group and DM+ICA II group were treated with vehicle or ICA II (5 mg/kg/day) for another 8 weeks, respectively. Then, blood creatinine, 24-hour urine protein, blood urea nitrogen, and glycosylated hemoglobin were measured, as well as the expression of von Willebrand factor, malondialdehyde, transforming growth factor-β/drosophila mothers against decapentaplegic protein/connective tissue growth factor (TGF-β/Smad/CTGF) signaling, marker of proliferation Ki-67, and EdU+ LRCs in renal tissues. Increased levels of creatinine, 24-hour urine protein, and blood urea nitrogen and remarkably decreased proportion of normal glomeruli and increased proportions of I, IIa, IIb, and III glomeruli were observed in diabetic rats, while ICA II could reverse these changes. Interestingly, ICA II could significantly downregulate the levels of malondialdehyde and TGF-β/Smad/CTGF signaling and increase the expression of von Willebrand factor, Ki-67, and EdU+ LRCs in the kidney. ICA II treatment could ameliorate diabetic nephropathy in STZ-induced diabetic rats by increasing endothelial cell contents, downregulating TGF-β/Smad/CTGF signaling pathway and oxidative stress level, and promoting cell proliferation both in kidney cortex and medulla. These beneficial effects appear to be mediated by its antioxidant capacity and recruitment of endogenous EdU+ progenitor cells into the kidney tissue. |
Mendeley readers
The data shown below were compiled from readership statistics for 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.
Geographical breakdown
| Country | Count | As % |
|---|---|---|
| Unknown | 28 | 100% |
Demographic breakdown
| Readers by professional status | Count | As % |
|---|---|---|
| Student > Bachelor | 6 | 21% |
| Student > Doctoral Student | 4 | 14% |
| Student > Master | 3 | 11% |
| Student > Ph. D. Student | 1 | 4% |
| Professor | 1 | 4% |
| Other | 0 | 0% |
| Unknown | 13 | 46% |
| Readers by discipline | Count | As % |
|---|---|---|
| Medicine and Dentistry | 6 | 21% |
| Pharmacology, Toxicology and Pharmaceutical Science | 5 | 18% |
| Biochemistry, Genetics and Molecular Biology | 3 | 11% |
| Agricultural and Biological Sciences | 1 | 4% |
| Unknown | 13 | 46% |
Attention Score in Context
This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 09 September 2015.
All research outputs
#17,286,645
of 25,374,917 outputs
Outputs from Drug Design, Development and Therapy
#1,105
of 2,268 outputs
Outputs of similar age
#165,909
of 276,789 outputs
Outputs of similar age from Drug Design, Development and Therapy
#64
of 133 outputs
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