The Complex Regulation of Tanshinone IIA in Rats with Hypertension-Induced Left Ventricular Hypertrophy

摘要: Tanshinone IIA has definite protective effects on various cardiovascular diseases. However, in hypertension-induced left ventricular hypertrophy (H-LVH), the signaling pathways of tanshinone inhibition remodeling and cardiac dysfunction remain unclear. Two-kidney, one-clip induced hypertensive rats (n = 32) were randomized to receive (5, 10, 15 mg/kg per day) or 5% glucose injection (GS). Sham-operated (n = 8) received 5%GS as control. Cardiac function dimensions assessed by using an echocardiography system. Histological determination fibrosis apoptosis was performed hematoxylin eosin, Masson’s trichrome TUNEL staining. Matrix metalloproteinase 2 (MMP2) tissue inhibitor matrix metalloproteinases type (TIMP2) protein expressions rat myocardial tissues detected immunohistochemistry. Rat cardiomyocytes isolated a Langendorff perfusion method. After 48 h culture, supernatant collected determine potential related proteins impact apoptosis. Compared with sham rats, heart H-LVH (5%GS) group suffered severely from oxidative damage, extracellular (ECM) deposition. In group, treated decreased malondialdehyde (MDA) content increased superoxide dismutase (SOD) activity. inhibited confirmed reduction positive down-regulation Caspase-3 activity Bax/Bcl-2 ratio. Meanwhile, plasma apelin level APJ receptor. suppressed through regulating paracrine factors released TGF-β/Smads pathway conclusion, our vivo study showed that could improve enhancing contractility, inhibiting ECM deposition, limiting damage.