Effect of Grape Seed Procyanidins on the Blood Pressure in Renovascular Hypertensive Rats and Its Mechanism
|School||Zunyi Medical College,|
|Course||Pathology and Pathophysiology|
|Keywords||grape seed procyanidins renovascular hypertensive rats eNOS ET-1 SOD MDA TNF-α IL-10|
Objective:To investigate the effect of grape seed procyanidins (GSP) on the blood pressure in renovascular hypertensive (RH) rats and its mechanism.Methods:2K1C method was used to establish the RH rat models. Meanwhile,8 rats were served as controls. After 2 weeks of operation,32 rats which tail systolic pressure increased above 130 mmHg were selected as successful RH rats, and divided into 4 groups (n=8) randomly:renovascular hypertensive model (RH model); low GSP treated (low GSP,50 mg·kg-1·d-1); high GSP treated (high GSP,200mg·kg-1·d-1) and captopril treated group (captopril,30 mg·kg-1·d-1). Tail systolic pressure was measured at the same time weekly. The activity of superoxide dismutase (SOD), malonaldehyde (MDA) and nitric oxide (NO) levels and total antioxidant capacity (T-AOC) in serum were determined respectively 6 weeks after treatment. ELISA was performed to detect the TNF-a and IL-10 levels in serum. Western blotting was used to evaluate the expressions of endothelial nitric oxide synthase (eNOS) and endothlin-1 (ET-1) in abdominal aortic tissues.Results:Compared with control group, the tail systolic pressure in RH model group was increased significantly 6 weeks after GSP treatment. In the RH model rats, treatment with GSP reduced the tail systolic pressure, MDA and TNF-a levels in serum and the expressions of ET-1 in abdominal aortic tissues, increased the activity of SOD, IL-10, NO levels and T-AOC in serum, as well as the expressions of eNOS in abdominal aortic tissues.Conclusion:GSP can decrease tail systolic pressure significantly of RH rats by increasing the antioxidative ability, the expressions of eNOS and NO production in vascular endothelial cells, inhibiting inflammatory mediator TNF-αand the expressions of ET-1, and increasing the level of anti-inflammatory mediator IL-10.