OBJECTIVETo observe the effects of Chinese materia medica (CMM) of qi benefiting, yin nourishing, stasis removing, and collaterals dredging (QBYNSRCD) and their dissembled recipes on nephrin of diabetes mellitus (DM) model rats.

METHODSThe DM model was induced by high fat diet combined with low dose STZ. Rats in the normal control group (abbreviated as Group N) and the model group (abbreviated as Group M) were administered with ultrapure water at corresponding volume by gastrogavage. Rats in the CMM of QBYNSRCD treatment group (abbreviated as Group YHT) were administered with CMM of QBYNSRCD, composed of milkvetch root, rehmannia root, danshen root, chuanxiong (2 packages each), solomonseal, earth worm, leech, and scorpion (1 package each), which was administered at 1.0 g/kg. Rats in the CMM of qi benefiting, yin nourishing, and stasis removing (QBYNSR) treatment group (abbreviated as Group YT) were administered with CMM of QBYNSR, composed of milkvetch root, rehmannia root, danshen root, chuanxiong (2 packages each), and solomonseal (1 package each), which was administered at 0. 92 g/kg. Rats in the CMM of qi benefiting, yin nourishing, and collaterals dredging (QBYNCD) treatment group (abbreviated as Group YT) were administered with CMM of QBYNCD, composed of milkvetch root, rehmannia root (2 packages each), solomonseal, earth worm, leech, and scorpion (1 package each), which was administered at 0.79 g/kg. The volume was set to 1 mL/100 g, once daily by gastrogavage, for total 32 weeks. Rats' body weight was measured. By the end of medication, urinary creatinine (UCr), 24-h urinary albumin (U-alb), and urinary nephrin (U-nephrin), fasting blood glucose (FBG), glycosylated hemoglobin (HbA1c), serum creatinine (SCr), and nephrin of kidney tissues homogenate (K-nephrin) were detected. The renal tissue sections were stained with Masson. The pathomorphological changes were observed.

RESULTSThe body weight of rats in Group N increased gradually. After modeling, the body weight of rats in Group M and all medicated groups obviously decreased. Compared with Group M, the decreased body weight was not obvious in all medicated groups, still showing statistical difference (P < 0.01). Compared with Group N, U-alb and U-nephrin in Group M significantly increased (P < 0.01) in a positive linear correlation (r = 0.941, P = 0.017). K-nephrin significantly decreased, and K-nephrin had a negative linear correlation with U-alb (r = -0. 987, P = 0.002). FBG, CCr, and HbA1c significantly increased (P < 0.01). Glomeruli were obviously enlarged under light microscope, with obviously increased extracellular matrix accumulation. Compared with Group M, corresponding indices were obviously improved ( P < 0.01) except FBG and HbA1c in Group YT. As for inter-group comparison among all medicated groups, the improvement of CCr was the best in Group YHT with statistical difference shown (P < 0.01). There was no statistical difference for the rest indices (P > 0.05). When compared with Group M, the hypertrophy of glomerulus was not so obvious in all medicated groups. Neither was extracellular matrix accumulation.

CONCLUSIONSCMM of QBYNSRCD and dissembled recipes showed renal protection on DM model rats. One of its action pathways might be reducing the loss of nephrin, thus reducing U-alb.