Objective: To explore the effects of rosmarinic acid （RA） on experimental mesangioproliferative glomerulonephritis （MsPGN） and renal TGF-β1 expression. Methods: Rabbit antithymocyte serum（ATS） was produced, and then MsPGN animal models were prepared in Sprague-Dawley rats by a single intravenous injection of ATS. Twenty-four rats were randomly divided into four groups（n = 6, respectively）: control group, treated with rabbit serum and tap water: model group, treated with ATS （10 ml／kg ） and tap water: low-dose and high-dose rosmarinic acid groups, treated with ATS（10 ml／kg ） and rosmarinic acid［25 mg／（kg·d）］ and ［25 mg／（kg·d）, respectively］. Rosmarinic acid was administered by gavage for 7 days from the day of serum injection. Urinary protein was examined. All rats were sacrificed on the 8th day, then the kidneys were collected. The morphologic lesions were observed by PAS stain, and the expression of TGF-β1 was detected by semi-quantitative RT-PCR and immunohistochemistry. Results:Compared to model group, the level of 24-hour proteinuria in low-dose or high-dose rosmarinic acid treated groups decreased significantly. Renal pathologic changes in rosmarinic acid treated groups was also improved. Compared to normal group, glomerular expression of TGF-β1 mRNA was significantly increased in model group（P < 0.01）, which was significantly inhibited by low-dose or high-dose rosmarinic acid. The expression of TGF-β1 mainly distributed along glomerular vessels and mesangiums. Compared to normal group, the expression of TGF-β1 was increased significantly in glomeruli of MsPGN rats. After 7 days of treatment, rosmarinic acid significantly down-regulated the expression of TGF-β1. Conclusion：Renoprotective mechanism of rosmarinic acid may partly be correlated with suppression on overexpression of TGF-β1 in renal tissue of MsPGN rats.