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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Su, Xuesong Yu, Rui Yang, Xu Zhou, Guangyu Wang, Yanqiu Li, Li Li, Detian |
| Description | Country affiliation: China Author Affiliation: Su X ( Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.); Yu R ( Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.); Yang X ( Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.); Zhou G ( Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.); Wang Y ( Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.); Li L ( Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.); Li D ( Department of Nephrology, Shengjing Hospital of China Medical University, Shenyang, China.) |
| Abstract | Peritoneal dialysis (PD) is an effective treatment for patients with end-stage renal diseases, but long-term continuous PD causes peritoneal fibrosis (PF). This study aims to evaluate the anti-fibrotic effect of telmisartan on a rat model of PF and to investigate the underlying mechanisms. Five-sixths kidney nephrectomy and PD were used to establish the PF rat model. Glucose (2.5%) was used to establish an in vitro model in rat peritoneal mesothelial cells (PMC). Haematoxylin-eosin staining was used to examine the structural alterations. Masson's trichrome staining was used to observe the tissue fibrosis in peritoneal membrane of rats. Real-time polymerase chain reaction was used to measure messenger RNA expressions of profibrotic factors. Western blotting was used to determine protein expressions of profibrotic factors, peroxisome proliferator-activated receptor-γ, and mitogen-activated protein kinases (MAPK). Results demonstrated that administration of telmisartan dose-dependently attenuated the thickening of the peritoneal membrane and the fibrosis induced by long-term PD fluid exposure in rats. In addition, telmisartan treatment inhibited the upregulation of profibrotic factors induced by PD in the peritoneum of rats and by high-concentration glucose in PMC. Telmisartan was also effective in inhibiting PD and high-concentration, glucose-induced phosphorylation of MAPK in the peritoneum and PMC. Furthermore, peroxisome proliferator-activated receptor-γ (PPARγ) inhibitor GW9662 blocked these protective effects of telmisartan in PMC. The results suggest that telmisartan is effective in attenuating PD-induced PF, and this effect may be associated with the inhibition of profibrotic factor expression and MAPK phosphorylation via PPARγ activation. |
| File Format | HTM / HTML |
| ISSN | 03051870 |
| Issue Number | 6 |
| Volume Number | 42 |
| e-ISSN | 14401681 |
| Journal | Clinical and Experimental Pharmacology and Physiology |
| Language | English |
| Publisher | Wiley-Blackwell |
| Publisher Date | 2015-06-01 |
| Publisher Place | Australia |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Discipline Physiology Discipline Pharmacology Angiotensin Ii Type 1 Receptor Blockers Therapeutic Use Benzimidazoles Benzoates Ppar Gamma Metabolism Peritoneal Fibrosis Prevention & Control Animals Cells, Cultured Dose-response Relationship, Drug Male Antagonists & Inhibitors Pathology Rats Rats, Sprague-dawley Journal Article Research Support, Non-u.s. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Physiology Physiology (medical) Pharmacology |
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