Reno-protective effects of atorvastatin independent of blood cholesterol lowering
10.3724/SP.J.1008.2010.00734
- Author:
Zhen-E XU
1
Author Information
1. Department of Nephrology
- Publication Type:Journal Article
- Keywords:
Atorvastatin;
CD36 antigens;
Class A scavenger receptors;
Glomerulosclerosis;
Hyperlipidemias;
Transforming growth factor beta
- From:
Academic Journal of Second Military Medical University
2010;31(7):734-738
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate whether atorvastatin can prevent renal injury in mice independent of the lipid-lowering effects. Methods: CD36-/- SR-A-/- ApoE-/- mice were randomly assigned to a high fat diet (high fat group) and high fat diet plus atorvastatin (atorvastatin) group; male C57BL mice with a chow diet served as controls. Terminal blood samples were taken for plasma cholesterol assay 14 weeks later. Renal sections were used for histological and immunohistochemistry assessments. The lipid accumulation in the kidney was evaluated by Oil Red O (ORO) staining. The mRNA expression of transforming growth factor-β (TGF-β), collagen I and IV, fibronectin, and α-smooth muscle actin (α-SMA) were analyzed by real-time PCR. Results: Blood total cholesterol levels (LDL-cholesterol and HDL-cholesterol) were not nd high fat group. Meanwhile, ORO staining showed that atorvastatin significantly different between atorvastatin group a decreased lipid accumulation in the kidney; Masson and H-E staining demonstrated that atorvastatin therapy attenuated massive structural changes, including mesangial proliferation, interstitial matrix deposition, accumulation of extracellular matrix proteins, tubular-interstitial inflammatory cell infiltration, and renal deformations with glomerulosclerosis/tubulointerstitial fibrosis in the high fat group. Moreover, atorvastatin therapy not only decreased TGF-β expression at mRNA and protein levels, but also decreased the expression of factors related to fibrosis. Conclusion: Atorvastatin can protect the kidney independent of the lipid-lowering effects and SR-A, CD36 receptor pathways, and it might be related to decrease of TGF-beta expression.
