Purpose: To determine the effects of rhynchophylline (Rhy) on the progression of cardiovascular diseases in rats.Methods: Wistar Kyoto (WKY) and spontaneously hypertensive rats (SHR, 7 week old, weighing 180 - 200 g) were used in this study. The rats were divided into WKY, SHR, SHR+ Rhy (30 mg/kg), and SHR+ Rhy (50 mg/kg). WKY rats were used as the normal control group which had free access to distilled water. The rats were then orally administered Rhy (30 and 50 mg/kg daily by gavage). For inhibition of PPARr, T0070907 was given at a dose of 2 mg/kg for 24 h. The blood pressure of control, spontaneously hypertensive rats (SHR), and SHR rhynchophylline (Rhy) rats were measured. While PPARr levels in the hypertensive rats were assessed by Western blot. Cell apoptosis in response to SHR and Rhy were evaluated by TdT-mediated dUTP nick-end labeling (TUNEL) and Western blot assays, whereas oxidative stress and inflammatory response in SHR rats treated with Rhy were determined by enzyme linked immunosorbent assay (ELISA) and Immunoblot assays, respectively.Results: Rhy decreased hypertension and up-regulated PPAR gamma in SHR rats (p < 0.01). In addition, Rhy improved SHR endothelial cell apoptosis by inducing PPAR gamma, and also produced reduction in proinflammatory factor secretion by inducing PPAR gamma. Furthermore, Rhy mitigated oxidative stress and iron death by inducing PPAR gamma (p < 0.001).Conclusion: Rhynchophylline provides a promising method in alleviating endothelial injury in SHR rats by modulating PPAR gamma-mediated inflammation and oxidative stres. We therefore thought Rhy alleviated endothelial injury and could serve as a promising drug.