Expression of LOX-1 in type 2 diabetic rat tubular interstitial tissues

AIM： To explore the effect of lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) on type 2 diabetic nephropathy in rats. METHODS：The Sprague-Dawley (SD) rats were randomly divided into control group and model group. The animal model was established by intraperitoneal injection of low-dose streptozotocin (STZ, 30 mg/kg) plus feeding with high-fat/high-glucose diets for one month. Biochemical parameters and 24 h urine album excretion rate (UAER) were monitored. The morphological changes of the renal tissue were examined under microscope with hematoxylin-eosin (HE) and periodic acid-Schiff reaction (PAS) staining. The protein levels of LOX-1 and transforming growth factor β1 (TGF-β1) in the renal tissues were determined by the method of immunohistochemistry. The mRNA expression of LOX-1 and TGF-β1 was detected by real-time polymerase chain reaction. The serum levels of monocyte chemotactic protein-1 (MCP-1), intercellular adhesion molecule (ICAM) and tumor necrosis factor α(TNF-α) were measured by enzyme-linked immunosorbent assay (ELISA). The correlation between LOX-1 and UAER, inflammatory factors and TGF-β1 was analyzed. RESULTS：Compared with normal group, total cholesterol (TC), triglyceride (TG), low-density lipoprotein (LDL) and UAER in model groups markedly increased, high-density lipoprotein (HDL) only increased at 0 week, then decreased at 4 and 8 weeks. The expression of LOX-1 and TGF-β1 at mRNA and protein levels was increased, as well as the concentration of serum inflammatory factors such as MCP-1, ICAM and TNF-α. The obvious relations between LOX-l mRNA with UAER, TNF-α and TGF-β1 were observed (r=0.509, 0.649 and 0.800, respectively, P<0.05). CONCLUSION：LOX-1 is significantly increased in type 2 diabetic rat tubular interstitial tissues and aggravates the dysfunction of renal tubules by releasing inflammatory factors and promoting inflammatory cell infiltration.