Effects Model Details Ref. Anti-coagulant effect Platelets exposed to ADP Inhibiting aggregation. [6 ] Rats Inhibiting thrombosis formation. [6 ] Blood sample from rabbits Inhibiting platelet aggregation induced by ADP and PAF and decreasing blood viscosity. [6 ] Blood sample from rabbits Inhibiting WRP aggregation and PMNs aggregation induced by PAF [7 ] Rabbit plasma Prolonging PT and RT. [8 ] Myocardial ischemia LAD-induced MI mice Reversing the haemodynamic changes including LVSP, +d p/d t and −d p/d t, enhancing the survival rate, increasing expressions of nucleolin and VEGF-A. [9 ] LAD-induced MI rats Reducing CK-MB, ROS, cTnI and 8-OHdG expression, and increasing SOD activity. [10 ] H9C2 cells subjected to OGD Reducing CK-MB, LDH, MDA, ROS and cell apoptotic number and increasing MMP, SOD activity, and expressions of PGC-1α and Nrf2. [11 ] ISO-induced MI rats Reducing CK-MB, LDH, MDA, ROS and cell apoptotic number, inhibiting cell apoptosis and increasing MMP, SOD activity and expressions of PGC-1α and Nrf2. [11 ] MI/R rats Reducing the infarct size and the release of LDH. [12 ] Ca2+ -induced ventricular myocytes Reducing mitochondria swelling, increasing phosphorylated eNOS protein and preventing cell death and depolarization of the mitochondrial membrane. [12 ] Cardiac myocytes stimulated by anoxia and reoxygenation Reducing cell viability and closed MPTP rods, and increasing opened MPTP round cells. [13 ] Cardiac myocytes introduced by ionomycin Increasing opened MPTP round cells and decreasing closed MPTP rods. [13 ] EPCs stimulated by SDF-1α Increasing CXCR4 expression. [14 ] MI mice caused by the ligation of left coronary artery Increasing EF, FS, EPC number, VEGF-A and SDF-1α and reducing apoptotic signals, TGF-β and Col I. [14 ] H9C2 exposed to H/R Reducing LDH, apoptosis index, Bcl-2/Bax ratio, cleaved Caspase-3 and increasing expression and activity of HO-1, Akt phosphorylation and Nrf2 translocation. [10 , 15 ] H9C2 exposed to H/R Increasing cell viability, ATP, Mn-SOD and HO-2 and reducing cyto c, MDA, LDH, apoptosis index and Caspase-3. [16 ] NRVMs subjected to H/R and LPS Increasing cell viability and reducing levels of TNF-α and IL-1β and expressions of TLR4 and NF-κ [17 ] MI/R rats accompanied hyperlipidemia trigged by high-fat diet Reducing TLR4 expression, infarct size, CK-MB and LDH activity. [17 ] Artery constriction SHR and the normotensive rats Reducing mAP and HR in vivo , and down-regulating LVSP, LVEDP, +d p/d [18 ] Immunized rats Reducing systolic BP, HR, ET, ox-LDL and NO and relieving the histological change in the thoracic aortic endothelium. [19 ] Aorta ring isolated from the immunized rats Enhancing the diastolic response induced by Ach and SNP and attenuating the vascular contractile effect of PE. [19 ] Rat thoracic aorta rings induced by PE Inhibiting IP3 receptor in VSMCs and thus reducing extracellular Ca2+ influx and intracellular Ca2+ release. [20 ] Ang II-stimulated rat adventitial fibroblasts Inhibiting proliferation and collagen synthesis and decreasing expressions of MMP-1, TGF-β 1, α -SMA and NF-κ [21 ] VSMCs exposed to PDGF-BB Reducing cell viability, cyclin D1, cyclin E, CDK2, CDK4, cGMP level and NO content and inhibiting phenotype switching and increasing HO-1 expression. [22 ] VSMCs induced by LPS Inhibiting proliferation and migration and down-regulating levels of TNF-α , IL-6 and IL-8. [23 ] PASMCs under hypoxia Inhibiting proliferation and cell cycle. [24 ] PAH rats induced by hypoxic Blocking the progression of pulmonary artery remodeling, decreasing the cell count in the small pulmonary bronchioles, attenuating right ventricular hypertrophy and decreasing mRVSP and protein expressions of PCNA and Ki67. [24 ] PE-induced rat PA Showing vasorelaxing effect independent of PA endothelium. [25 ] PAH rats stimulated by MCT Reducing RVSP, mPAP, RV/LVPS, the mean percent wall thickness of pulmonary arterioles and the vascular muscularization and increasing expressions of IL-1β , IL-6 and TNF-α in the mRNA level and SOD activity and decreasing levels of MDA and 8-OHdG. [26 ] Cardiac hypertrophy Overload-induced cardiac hypertrophy rats induced by the ligation of abdominal aorta Reducing LVMI, inhibiting cell apoptosis by up-regulating Bcl-2/Bax ratio and decreasing expressions of MMP-2 and MMP-9. [27 ]
