Objective Our previous study had proved that long-term atorvastatin administration notably improves the pathological aging changes of kidney. The aim of this study was to find the underlying mechanism of different doses atorvastatin in attenuation of the aging changes in the kidneys. Methods Twenty-month-old normal female Wistar rats were divided into 3 groups (n=9 for each group), that is, aged control group, large and small dosed atorvastatin groups. The rats from the corresponding groups were treated with normal saline, or atorvastatin at 10 or 1 mg/(kg?d) respectively through intragastrical injection for 4 months. All rats were sacrificed at the end of treatment, and another 9 rats at the age of 3 months served as normal controls. The expression of matrix metalloproteinase (MMP-9, -2), tissue inhibitors of metalloproteinase (TIMP-1, -2), transforming growth factor-b1 (TGF-b1) and peroxisome proliferators activated receptors (PPARs) at mRNA and protein levels in the kidney tissues were detected by RT-PCR and Western blotting respectively. Results The rats at 24 months old had significantly increased expression of MMP-9 and TGF-b1 than those at 3 months old (P<0.05, P<0.01). But no change was found in the expression of TIMPs and PRARs between them. Atorvastatin reversed these above changes. It resulted in a decrease in the increased expression of MMP-9 and TGF-b1, and an increase in the downregulated expression of TIMP-1, PPARα, PPARβ and PPARγ (P<0.01, P<0.01, P<0.05). Conclusion Imbalanced expression of MMPs/TIMPs exists in the aging rat kidney, with up-regulation of TGF-b1. Long-term treatment of atorvastatin rebalances MMPs/TIMPs expression through downregulating MMP-9, upregulating TIMP-1, and decreasing TGF-b1 expression, and thus attenuates the aging changes in the kidneys. Further study is needed to identify whether atorvastatin-induced activation of PRARs plays roles in the process.