Objective       To investigate the correlation between monocyte chemotactic protein-1 (MCP-1) expression and oxidative stress indices in kidney of type 2 diabetic nephropathy (DN) rat model

and through probucol early intervention to explore the protective mechanism of antioxidants on diabetic kidney.      Methods       Twenty-four male Wistar rats of 8 weeks age were randomly divided into a normal control group (n=6) and a model group (n=18). Rats of the normal control group were fed with regular diet

while rats of the model group were fed with high-fat high-sugar diet and 4 weeks later were given an intraperitoneal injection of 35 mg/kg streptozotocin (SZT). The successfully constructed type 2 diabetic nephropathy rat models were then randomly divided into a DN group (n=5)

a P group (n=6) and an A group (n=6). Rats of the P group were given 61 mg/kg Probucol and high-fat high-sugar diet. Rats of the A group were given 200 mg/kg Apocynin (NAPDH oxidase inhibitor) and high-fat high-sugar diet. At week 12

the levels of 24-hour urine protein

urinary micro albumin

serum creatinine and blood urea nitrogen were measured. The rats were then sacrificed. Renal and ultrasturctural pathological changes were examined. Renal tissue NT and MCP-1 expressions were measured by immunohistochemical assay. NF-κB mRNA expression was semi-quantified by RT-PCR

and correlation analysis was performed.      Results        ①Compared with the DN group

the P group and A group had significantly lower levels of urinary micro albumin

serum creatinine

blood urea nitrogen and kidney hypertrophy index (P0.05). ②MCP-1 expression in the DN group was positively correlated with NT expression and renal function (r=0.0); both MCP-1 and NT levels were significantly higher than those in the N group (P0.05). ③NT and MCP-1 expressions in the P group were significantly decreased as compared with those in the DN group (P0.05)

but not significantly different from those in the A group.      Conclusion       Antioxidant may down-regulate MCP-1 expression through inhibition of oxidative stress in diabetic nephropathy and therefore protect renal function by reducing injury resulted from MCP-1 overexpression.