| Summary: | This study aimed to examine the effects of atorvastatin on early hypertensive renal damage and explored the underlying mechanisms. 12-week-old salt-loaded spontaneous hypertensive rats (SHRs) were divided into four groups: atorvastatin (AVT), losartan potassium (LP), atorvastatin combined with peroxisome proliferators-activated receptor γ (PPAR-γ) inhibitor (AVT + GW9662), and saline. During 10 weeks administration blood pressure and urea albumin creatinine ratio were determined. We also examined the renal function, pathological changes of kidney, inflammatory cytokines in the serum and the association of the change of inflammatory factors in the kidney tissue. AVT did not reduce the mortality of the SHRs. AVT reduced the blood pressure of SHRs, but the effect was not comparable to that of LP. AVT significantly decreased urine protein. AVT and LP displayed comparable effects by significantly decreasing inflammatory cytokines (hs-CRP, IL-1β, IL-6, TNF-α, and TGF-β) levels in serum. AVT and LP both apparently improved renal pathological changes and significantly reduced the infiltration of macrophage in renal tubular interstitial. Both mRNA and protein expression levels of TLR4, NFκB, MCP-1 were significantly down regulated in AVT and LP groups. There was no significant change in macrophage polarity. The addition of PPAR-γ inhibitor partially reduced the anti-inflammatory effect of AVT. These results mean that Atorvastatin can alleviates the pathology of hypertensive renal damage. Atorvastatin protects the kidney by reducing the apparent inflammation in salt-loaded SHRs. Atorvastatin alleviates inflammation partially by augmenting expression of PPAR-γ.
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