Objective        To explore the effect of mangiferin on the renal interstitial fibrosis induced by high fructose in spontaneously hypertensive rats (SHRs).       Methods        Twenty-four SHRs were randomly divided into 4 groups: control group

fructose group

fructose + mangiferin (5 mg/kg) and fructose + mangiferin (15 mg/kg) groups. After 7-week feeding

the rats were sacrificed

and blood samples were collected for determination of plasma concentrations of glucose

total cholesterol

triglyceride and non-esterified fatty acid. The triglyceride level in the kidneys was determined histologically and enzymatically. The renal interstitial fibrosis was observed by Masson staining. The mRNA expression levels of monocyte chemoattractant protein-1 (MCP-1)

CD68

α-smooth muscle actin (α-SMA)

collagen alpha-4 (Ⅳ) chain (col4a4)

transforming growth factor-beta (TGF-β)

plasminogen activator inhibitor-1 (PAI-1) and urokinase plasminogen activator (uPA) in the kidney were detected by real-time PCR

and the protein expression levels of uPA and PAI-1 were examined by immunohistochemistry.       Results      Compared to the control group

the renal interstitial fibrosis was increased in the fructose group (P0.01)

and mangiferin (15 mg/kg) could significantly reduce the fibrosis induced by fructose (P0.05). There was no marked change in renal triglyceride among the 4 groups

and the mRNA expressions of MCP-1

CD68

α-SMA

col4a4

and TGF-β in the kidneys also had no change. Mangiferin (15 mg/kg) apparently reversed the fructose-induced uPA/PAI-1 mRNA ratio reduction

and decreased the over-expression of PAI-1 protein induced by fructose.       Conclusion        Mangiferin can alleviate renal interstitial fibrosis induced by high fructose in the SHRs

which may be related to modulation of renal PAI-1 and uPA.