Protective effect of Sunset Abelmoschus on podocyte injury in adriamycin?induced nephropathy rats

Objective To explore the effect of Sunset Abelmoschus on podocyte injury in adriamycin?induced nephropathy rats. Methods Fifty male SD rats were randomly divided into five groups: sham operation group (n=10), model group (n=10), Sunset Abelmoschus low dose group (0.5 g?kg-1?d-1 n=10), middle dose group (1.0 g?kg-1?d-1, n=10) and high dose group (2.0 g?kg-1?d-1, n=10). Unilateral nephrectomy combined repeated adriamycin injection were performed to establish adriamycin?induced nephropathy models. The rats were administered with the corresponding dose of Sunset Abelmoschus during the experiment period. Urinary protein, urinary N?acetyl glucose aminotransferase (NAG), serum albumin, serum creatinine and blood lipid were measured before operation and 2, 4, 6, 8 weeks after operation. The rats were sacrificed on week 8 for the renal histological examination, including light microscope and electron microscope. Expression of nephrin was examined by immunofluorescence assays. Results As compared to model group, urinary protein and NAG significantly decreases in Sunset Abelmoschus groups in each time point, especially in high dose group (P<0.01), meanwhile the serum albumin increased and the disturbance of lipid metabolism was improved in Sunset Abelmoschus groups (P<0.05). Compared with sham group, Scr increased significantly in model group and Sunset Abelmoschus groups at the 4th week. At the 8th week, Scr in high dose group was lower than that in model group (P<0.05), and the ratio of glomerular globe sclerosis and segmental sclerosis, tubulointerstitial damage reduced in Sunset Abelmoschus groups, especially in high dose group. The podocyte damage and the extent of foot process fusion were improved in Sunset Abelmoschus groups compared with model group. Expression of nephrin increased in Sunset Abelmoschus groups than that in model group. Conclusion Sunset Abelmoschus can ameliorate proteinuria and renal tissue damage of adriamycin?induced nephropathy rats, whose mechanism may be associated with the improvement of podocyte injury.