BACKGROUND: As an important factor causing end-stage renal disease, diabetic nephropathy is correlated with low-grade chronic inflammation and immune system activation. This study aimed to investigate the protective function of puerarin on the kidneys of diabetic rats.

MATERIAL AND METHODS: A cohort of healthy male SD rats (7 weeks old) were randomly divided into a control group, a model group, and a puerarin treatment group with high (H), moderate (M), and low (L) dosage. After streptozotocin induction, puerarin was applied via intragastric administration for 8 consecutive weeks with dosages of 0.25, 0. 5 and 1.0 mg/(kg·d) for L, M, and H groups, respectively. Fasting blood glucose (BG), creatinine (Scr), urea nitrogen (BUN), and urine albumin excretion rate (UAER) were measured, along with morphological observation of renal cells. The expression of intracellular adhesion molecule 1 (ICAM-1) and tumor necrosis factor α (TNF-α) was determined using immunohistochemical (IHC) staining, while renal cortex cell apoptosis was assayed by in situ end-labeling method.

RESULTS: Model rats had significantly elevated levels of BG, Scr, BUN, and UAER compared to controls (p<0.05). All these increases were partially but significantly suppressed by puerarin (p<0.05), which also caused marked improvement of histopathological damages. Puerarin at each dosage significantly eliminated elevations of ICAM-1 and TNF-α levels in model rats (p<0.05), and decreased apoptotic indexes of renal cortex cells (p<0.05).

CONCLUSIONS: Early-stage renal damages can be significantly improved by puerarin, possibly via its suppression of ICAM-1 and TNF-α expression in diabetic rat kidneys.

Keywords: Blood Glucose - metabolism, Blood Urea Nitrogen, Creatinine - blood, Diabetes Mellitus, Experimental - metabolism, Diabetic Nephropathies - prevention & control, Dose-Response Relationship, Drug, Intercellular Adhesion Molecule-1 - biosynthesis, Isoflavones - pharmacology, Kidney - pathology, Random Allocation, Tumor Necrosis Factor-alpha - biosynthesis