Abstract:Objective To investigate the effect of gastrodin on ventricular remodeling in hypertensive rats with left ventricular hypertrophy (LVH) and its mechanism of action based on the Ras homolog gene family, member A (RhoA)/Rho-associated kinase (ROCK) pathway. Methods A total of 100 male Sprague-Dawley rats were randomly divided into sham-operation group, model group, low-, middle-, and high-dose gastrodin groups (at doses of 16, 24, and 32 mg/kg, respectively), and enalapril group (1.5 mg/kg), with 15 rats in each group. A rat model of LVH was established by the abdominal aorta constriction method. ELISA was used to measure the serum levels of angiotensin Ⅱ (AngⅡ) and interleukin-6 (IL-6); left ventricular hypertrophy index (LVHI) was calculated; hematoxylin and eosin staining and Masson staining were used to observe histomorphological changes of the myocardium; qRT-PCR and Western blot were used to measure the mRNA and protein expression of RhoA and ROCK in myocardial tissue. Results Compared with the sham-operation group, the model group had significant increases in systolic pressure of the caudal artery, LVHI, and serum levels of AngⅡ and IL-6 (P<0.05), a higher degree of myocardial fibrosis, and significant increases in the mRNA and protein expression levels of RhoA and ROCK (P<0.05). Compared with the model group, the low-, middle-, and high-dose gastrodin groups and the enalapril group had significant reductions in systolic pressure of the caudal artery, LVHI, and serum levels of AngⅡ and IL-6 (P<0.05), a lower degree of myocardial fibrosis, and significant reductions in the mRNA and protein expression levels of RhoA and ROCK (P<0.05). The enalapril group had the lowest mRNA and protein expression levels of RhoA and ROCK in myocardial tissue, and gastrodin exerted an effect in a dose-dependent manner. Conclusion Gastrodin can effectively reduce blood pressure of the caudal artery, LVHI, and serum levels of AngⅡ and IL-6 and improve ventricular remodeling in hypertensive rats, possibly by inhibiting the RhoA/ROCK signaling pathway.