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To explore the protective effect of glycyrrhizin in rats with nephrotic syndrome (NS) induced by adriamycin (ADR). 36 Sprague Dawley (SD) male rats were divided into control, untreated and glycyrrhizin treatment groups. The NS rat model was established by injecting ADR twice in the untreated and in the glycyrrhizin treatment groups. Rats in the glycyrrhizin treatment group were fed glycyrrhizin by intragastric administration for 7 days. Changes in the following indices were observed in the three groups before and 4 weeks after the treatment: 24 h urine protein quantitation (UPr), serum cholesterol (Ch), serum albumin (Alb), blood urea nitrogen (BUN), serum creatinine (sCr), laminin (LN), fibronectin (FN), collagen (Col), transforming growth factor beta1 (TGFbeta1) and connective tissue growth factor (CTGF); histopathology by light and electron microscope. Expression of LN, FN, ColIV, TGFbeta1 and CTGF in the cortex of the kidney were detected by semi-quantitative immunohistochemical analysis. Expression of TGFbeta1 and CTGF in the cortex of the kidney was detected by Fluorescein Based Quantitive RT-PCR. Macrophage infiltration was evaluated by the immunoperoxidase staining. Compared with the control group, 24 h UPr, Ch, BUN and sCr of rats in the untreated group were increased. Glycyrrhizin reduced 24 h Upr, Ch, BUN, sCr, LN, FN, Col, TGFbeta1, CTGF, and mean arterial blood pressure. Pathological changes in the kidney, the expression of LN, FN, Col, TGFbeta1 and CTGF in the cortex of the kidney in the glycyrrhizin treatment group were decreased compared with the untreated group. Glycyrrhizin also suppressed macrophage infiltration in the kidneys of NS rat models. Glycyrrhizin exerts protective effects in rats with NS, reducing the excretion of Upr, Ch, BUN, sCr, and mean arterial blood pressure, and also decreasing expression of LN, FN, Col, TGFbeta1 and CTGF in the kidney. Renal function is improved and the severity of NS is lessened.