ABSTRACT
BACKGROUND:Studies have found that β-casomorphin 7 can lessen oxidation of renal tubular epithelial cels and lower blood sugar in a rat model of diabetes. There is a few studies concerning the effect of β-casomorphin-7 on diabetic nephropathy. OBJECTIVE:To explore the effects of β-casomorphin-7 on renal injury in a rat model of diabetic nephropathy. METHODS:The 30 rats were equaly and randomly divided into control group, model group andβ-casomorphin-7 group. Twenty rat models of diabetes were established. In the model and β-casomorphin-7 groups, rats were intraperitonealy injected with streptozotocin (60 mg/kg). In the control group, rats were intraperitonealy injectedwith an equal volume of citric acid. Rats in the β-casomorphin-7 group were intragastricaly administeredβ-casomorphin-7 for 30 days. Rats in the model and control groups were given an equal volume of saline by intragastric administration. RESULTS AND CONCLUSION: (1) Compared with the control group, insulin levels decreased, glucagon, blood glucose, urine glucose, urine protein, serum creatinine, serum urea nitrogen levels, mRNA and protein expression levels of type I colagen and type IV colagen in kidney increased in the model group. (2) Compared with the model group, above indexes were apparently recovered in the β-casomorphin-7 group. These findings indicate that β-casomorphin-7 has a protective effect on renal injury in diabetic nephropathy rats.
ABSTRACT
BACKGROUND: Safflower yel ow is known to treat diabetic nephropathy, can protect kidney function, reduce lesions, delay or prevent the development of diabetic nephropathy. OBJECTIVE: To further verify the effects of safflower yel ow on the kidney in rats with diabetic nephropathy and the impact of safflower yel ow on the expression of renal cel receptor of angiotensin II1. METHODS: Thirty rats were equally and randomly divided into three groups: normal control group, model group and experimental group. In the experimental group and model group, rat models of diabetic nephropathy were established. At 1 week after model establishment, rats were daily intraperitoneally given safflower yellow injection 27.8 mg/kg, once a day. In the model and control groups, rats were daily intraperitoneally given an equal volume of saline. All rats were administered for 23 weeks. The kidney-related biochemical indicators and pathological changes in kidney tissue and the expression of angiotensin II1 type receptor on kidney tissue of rats were observed. RESULTS AND CONCLUSION: (1) Hypertrophy index of experimental group and model group was significantly higher than that of control group (P < 0.05). (2) 24-hour proteinuria, glycosylated hemoglobin, total cholesterol, triglycerides, creatinine and urea nitrogen of model group were higher than that of control group (P < 0.05). 24-hour proteinuria, glycated hemoglobin, total cholesterol and urea nitrogen in experimental group were higher than that of control group (P < 0.05). 24-hour proteinuria, total cholesterol, triglycerides, creatinine and urea nitrogen in the experimental group were lower than that of model group (P < 0.05). (3) Glomerular hypertrophy, thickening of capillary basement membrane, cell proliferation, and mesangial widening were detected in the model group. Abnormal changes in the kidney structure were found in the control group. The extent of damage of kidney of histopathology in the experimental group was between the control group and the model group. (4) The expression level of angiotensin receptor II1 of experimental group and model group was higher than that of control group (P < 0.05). The expression level of angiotensin receptor II1 of experimental group was lower than that of model group (P < 0.05). These results indicated that safflower yellow has a protective effect on diabetic nephropathy; the mechanism of action may be associated with blocking kidney partial renin-angiotensin system.