Protective effect of glycyrrhizin on nephrotic syndrome induced by adriamycin in rats.
OBJECTIVE
To explore the protective effect of glycyrrhizin in rats with nephrotic syndrome (NS) induced by adriamycin (ADR).


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Bi
Xuecheng
X
Guangzhou First Municipal People's Hospital, Affiliated Guangzhou Medical College, Guangzhou 510180, China.
Zhu
Gang
G
Han
Zhaodong
Z
Ye
Yongkang
Y
Liang
Yuxiang
Y
Zhang
Lei
L
Hao
Zhihong
Z
Zeng
Guohua
G
He
Huichan
H
Zhong
Weide
W
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use*; D000903:Antibiotics, Antineoplastic / Q000633:toxicity; D004317:Doxorubicin / Q000633:toxicity; D019695:Glycyrrhizic Acid / Q000494:pharmacology / Q000627:therapeutic use*; D007150:Immunohistochemistry; D007672:Kidney Cortex / Q000187:drug effects / Q000473:pathology; D008297:Male; D009404:Nephrotic Syndrome / Q000139:chemically induced* / Q000188:drug therapy* / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction
D000893:Anti-Inflammatory Agents; D000903:Antibiotics, Antineoplastic; D019695:Glycyrrhizic Acid; D004317:Doxorubicin