Aim of study:To examine the effects of active components of Radix Scrophulariae (ACRS) on ventricular remodeling in spontaneously hypertensive rats (SHR) and the underlying mechanism.Material and methods:ACRS contains Harpagide 18.7%,Harpagoside 13.4%,cinnamic acid 5.7%,angoroside C 14.6%.The the remaining constituents are mainly saccharides.The spontaneously hypertensive rats (SHRs) were divided into five groups:SHR control,SHR + 40 mg/kg captopril,SHR + 70 mg/kg ACRS,SHR + 140 mg/kg ACRS,SHR + 280 mg/kg ACRS.Normotensive age-matched WKY rats were assigned to two groups:WKY control,WKY + 140 mg/kg ACRS.After treatment with the corresponding agents or drinking water by gavage for 21 weeks,blood pressure,heart weight indexes and myocardium collagen deposition were observed.Results:When compared with WKY rats,SHR exhibited obvious higher blood pressure,higher heart weight indexes,more interstitial and perivascular collagen deposition.ACRS significantly lowered the blood pressure,decreased the heart weight indexes,inhibited the interstitial and perivascular collagen deposition,attenuated the collagen of types Ⅰ and Ⅲ accumulation,reduced the tissue angiotensin Ⅰ (Ang Ⅱ),serum norepinephrine and tumor necrosis factor-a (TNF-a) concentrations,attenuated TGF-pi and ACE mRNA over expression and the phosphorylation of ERKl/2 Thr202_Tyr204,JNK Thr183-Tyr185 and p38 MAPK Thr180-Tyr182.There were no significant differences of the above observed main values between WKY control group and WKY + 140 mg/kg ACRS group.Conclusions:ACRS could prevent ventricular remodeling in SHR.The mechanisms may be related to downregulating the mRNA expressions of collagen type Ⅰ,transforming growth factor-β1 (TGF-β1) and angiotensin converting enzyme (ACE),suppressing the phosphorylation of extracellular signal regulated kinase 1/2 (ERK1/2),c-Jun N-terminal kinase (JNK/SAPK) and p38 mitogen-activated protein kinases (p38 MAPK).