Protective effect of tongxinluo superfines on angiotensin II caused renal injury in rat.
- Author:
Ling-yan YUAN
1
;
Hong-qi ZHANG
;
Dan-ling XU
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; metabolism; Animals; Apoptosis; drug effects; Drugs, Chinese Herbal; pharmacology; Endothelium, Vascular; drug effects; metabolism; Kidney; blood supply; pathology; Male; NADPH Oxidases; metabolism; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; metabolism; Tumor Suppressor Protein p53; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2009;29(12):1104-1109
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the renal protective effect of Tongxinluo (TXL) and its mechanism of action.
METHODSEight-week old SD rats were divided into the sham-operated group (A), the model group (B) and the TXL group, 6 rats in each group. Angiotensin II (Ang II) was administered slowly (200 ng/kg per min) to rats in group B and C via subcutaneously embedded osmotic pump to make them stimulative model of renal injury, while to rats in group A, pump embedding with saline infusion. After modeling, TXL was given to group C by gastric perfusion in dosage of 0.8 g/kg per day. And the following indexes were observed 14 days later: configuration of renal arterial endothelium by transmission electron microscope; pathologic figure of kidney with HE stain; renal apoptosis by TUNEL; expression of p53 and p22phox by RT-PCR;and level of reactive oxygen species (ROS) in kidney.
RESULTSDifferent degree of congestion, swelling, denudation of endothelial cell in renal arterial endothelial cell; glomerular matrix proliferation and partial glomerular atrophy with tendency of fibrosis; increased renal parenchymal apoptosis; enhanced expression of p53 and p22phox; and elevated ROS were found in model animals. All the above-mentioned abnormalities, including glomerular injury, renal cell apoptosis, as well as the increased p53, p22phox expressions and ROS production were all alleviated in group C after TXL treatment.
CONCLUSIONTXL could protect renal against Ang II injury, and it may be realized by inhibiting NADPH-ROS/p53 pathways and suppressing cell apoptosis in renal parenchyma.