Objective: To observe the effects of Shenqi Compound (SQC) on the mRNA expression of angiotensin II type 1 receptor (AT1R) in the aorta of Goto-Kakizaki (GK) rats.
Methods: Totally 67 GK rats were randomly divided into 5 groups, i.e., the GK group (n =18), the model group (n =16), the atorvastatin group (n =17), and the SQC group (n =16). Another a normal control group was set up (n =18). The diabetic macrovascular disease model was prepared by adding L-NAME (at the daily dose of 0.10 mg/mL) in drinking water for GK rats. GK rats, except those in the normal control group were fed with high fat diet. Atorvastatin (at the daily dose of 1.60 mg/kg) and SQC (at the daily dose of 1.44 g/kg) were respectively administered by gastrogavage, once daily for 35 successive days. The blood glucose was determined by glucose oxidase method once per week. After 5-week medication, the contents of triglyceride (TG) and total cholesterol (TC) were determined by ELISA. The serum concentrations of angiotensin I (Ang II) were determined by RIA. The mRNA expression of AT1R in the aorta was determined by real-time quantitative reverse transcriptase PCR (RT-PCR).
Results: The blood glucose level was obviously lower in both the atorvastatin group and the SQC group after 4 weeks of medication (P <0.05). Besides, it was significantly lower in the SQC group than in the model group by the end of the 4th week (P <0.05). The concentrations of TG, TC and serum Ang II , and the mRNA expression of AT1R in the aorta were significantly higher in the model group than in the normal control group (P <0.01). After 5-week medication, the concentrations of TG, TC and serum Ang I , and the mRNA expression of AT1 R in the aorta were significantly lower in the atorvastatin group and the SQC group than in the model group (P <0.01, P <0.05). The mRNA expression of AT1R was significantly higher in the SQC group than in the atorvastatin group (P <0.05).
Conclusions: SQC could significantly reduce the levels of blood glucose, TG, TC, down-regulate the mRNA expression of AT1R in the aorta, and decrease the expressions of serum Ang II of GK rats with diabetic macrovascular disease. AT1 R might be one of effective targets of SQC in treating diabetic macrovascular diseases.