OBJECTIVETo study the effects of modified danggui buxue decoction (MDBD) on podocytes in adriamycin-induced nephropathy (DN) model rats.

METHODSSD rats were divided into four groups, i.e., the normal control group, the model group, the benazepril group, and the MDBD group. On the 7th, 28th, 42nd, and 56th day of modeling, the urine sample was collected to examine the dynamic changes of urinary albumin quantitation. The renal tissue was processed for the examinations under light microscope and electron microscope. The immunofluorescence of nephrin and podocin were detected. The expressions of the slit membrane expression protein in the renal tissue were further analyzed using RT-PCR and Western blot.

RESULTS(1) Urinary protein (UP): The UP did not obviously decrease in each treatment group on the 7th day, but it decreased so markedly on the 28th, 42nd, and 56th day. There was statistical difference in UP of the benazepril group and the MDBD group when compared with that of the model group (P < 0.05). The decrease was most obvious in the MDBD group. (2) Effects on the podocytes and the renal tissue:

RESULTSunder light microscope and electron microscope showed, when compared with the model group, the proliferation of mesangial cells, the renal tubule-interstitial lesion, the podocyte fusion, and the expressions of nephrin and podocin were milder, and the urinary albumin quantitation was more obviously reduced in the benazepril group and the MDBD group. But the renal fibrosis correlated renal pathological progress also existed, indicating the renal lesion degree was milder but could not be reversed. (3) Results of RT-PCR and Western blot: Statistical difference existed in the expressions of nephrin and podocin between the benazepril group and the MDBD group on the 56th day, when compared with the model group (P < 0.05).

CONCLUSIONMDBD showed therapeutic effects on adriamycin-induced nephropathy model rats. Its actions could be achieved through reducing albuminuria, inhibiting the proliferation of mesangial cells, attenuating the renal tubule-interstitial lesion, and protecting the integrity of the slit membrane structure.