Effects of Shenkangwan on renal expressions of angiotensin II and its type I receptor in rats with early diabetic nephropathy.
- Author:
Hai-bo LONG
1
;
Hong-xin NIU
;
Xiao-yun LI
;
Zhao-zhong XU
;
Hui ZHANG
;
Juan ZHONG
;
Lian-bo WEI
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; genetics; metabolism; Angiotensin II Type 1 Receptor Blockers; therapeutic use; Animals; Diabetic Nephropathies; drug therapy; metabolism; Drugs, Chinese Herbal; therapeutic use; Kidney; metabolism; Male; Phytotherapy; RNA, Messenger; genetics; metabolism; Rats; Rats, Sprague-Dawley; Receptor, Angiotensin, Type 1; genetics; metabolism
- From: Journal of Southern Medical University 2010;30(4):805-809
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effects of Shenkangwan on the expressions of angiotensin II (AngII) and its type I receptor (AT(1)R) and the renalprotection mechanism of Shenkangwan in rats with early diabetic nephropathy (DN).
METHODSThe rat models of DN established by a single injection of streptozotocin were randomly divided into 4 groups, namely the model group, Shenkangwan treatment group, irbesartan treatment group, and Shenkangwan and irbesartan treatment group, with normal rats as the control. All the rats received daily gavage for 8 weeks. The urinary protein quality in 24 h and plasma and renal contents of AngII were measured. The expressions of AT1R at the protein and mRNA levels in the kidney tissues were measured by immunohistochemistry and reverse transcription-polymerase chain reaction, respectively. The pathological changes of the kidney were observed microscopically.
RESULTSIn DN rats, Shenkangwan reduced the urinary protein quantity in 24 h and the contents of AngII in the plasma and kidney tissues, decreased the renal expressions of AT(1)R protein and mRNA, and alleviated the morphological damage of the kidney.
CONCLUSIONSShenkangwan offers renalprotection against DN probably by reducing the contents of AngII in the plasma and kidney tissues and inhibiting renal AT(1)R expressions.
