1) The protective effect of on myocardial infarction: The myocardial infarction (MI) model in rats was constructed by coronary ligation, and the protective effect of salvianolic acid B on MI was investigated. The results showed that compared with the control group, salvianolic acid B could exert a significant cardioprotective effect on MI. Mechanistic studies have shown that salvianolic acid B mainly inhibits the up-regulation of leptin and endothelin-reactive oxygen species (ET-ROS) and restores myocardial sarcoplasmic reticulum calcium ATPase 2a (sarco/endoplasmicreticulum ATPase 2a, SERCA2a) and phosphorus receptors in the myocardium. The normal expression of the protein, and then play a role in protecting the heart.
2) The protective effect of on MI/R injury: a large number of free radicals will be generated during MI/R, which will enhance the lipid peroxidation of cell membranes, change membrane fluidity and permeability, and lead to abnormal electrophysiological activities. , induce and promote arrhythmia. Due to the enhanced lipid peroxidation in myocardial cells, the content of peroxidation products such as malondialdehyde (MDA) in the myocardial ischemia area increases; lactate dehydrogenase (LDH) and creatine phosphokinase in coronary effluent (creatinephosphokinase, CPK) increased and myocardial tissue superoxide dismutase (superoxidedismutase, SOD) decreased. The study found that salvianolic acid B can significantly increase the SOD activity in myocardial tissue of MI/R-injured rats, and can effectively resist the toxic effect caused by oxygen free radicals, thereby reducing myocardial cell damage. The protective effect of salvianolic acid B on MI/R injury was investigated by constructing a rat MI/R model, and it was found that compared with the control group, administration of salvianolic acid B could significantly increase the levels of troponins (CTn) and creatine in plasma. The content of kinase isoenzyme (creatinekinase-MB, CK-MB), while significantly reducing the levels of nitric oxide (nitricoxide, NO) and total superoxide dismutase (total superoxide dismutase, TSOD) in plasma, indicating that Rat MI/R injury has obvious protective effect. Further research found that salvianolic acid B can alleviate oxidative stress, reduce calcium overload and improve endothelial function.
3) Has the effect of inhibiting cardiomyocyte hypertrophy: The effect of salvianolic acid B on angiotensinⅡ (AngⅡ)-induced cardiomyocyte hypertrophy in neonatal rats was investigated. The results showed that salvianolic acid B could inhibit AngⅡ Induced cardiomyocyte hypertrophy, decreased atrial natriuretic peptide and brain natriuretic peptide mRNA expression and decreased cell surface area. Mechanistic studies found that salvianolic acid B could inhibit the activity of poly(ADP-ribose)polymerase-1 (PARP-1); at the same time, it was found that overexpression of PARP-1 could attenuate the activity of salvianolic acid B Anti-cardiomyocyte hypertrophy effect, these studies show that salvianolic acid B has a good inhibitory effect on cardiomyocyte hypertrophy.
4)Can inhibit the formation of atherosclerosis: The effect of salvianolic acid B on atherosclerosis was investigated through experiments, and the results showed that the treatment of vascular smooth muscle cells with salvianolic acid B can effectively inhibit platelet-derived growth factor ( platelet-derived growth factor, PDGF)-induced cell proliferation and migration, and can significantly increase the expression of heme oxygenase-1 (hemeoxygenase-1, HO-1); at the same time, salvianolic acid can significantly reduce reactive oxygen species (reactive oxygen species) , ROS) production and reduction of nicotinamide adenine dinuclear
The ratio of nucleotide phosphate/reduced nicotinamide adenine dinucleotide phosphate (NADP/NADPH). Using human umbilical vein endothelial cells, it was found that salvianolic acid B can significantly induce the production of HO-1, and at the same time effectively inhibit the activation of nuclearfactor-κB (NF-κB) induced by tumor necrosis factor-α (TNF-α). Inhibition of HO-1 expression by siRNA abolished the protective effect of salvianolic acid on vascular endothelial cells and blocked the proliferation, migration and inflammation of HO-1-deficient cells. Further mechanism studies have shown that salvianolic acid B induces the expression of HO-1 by activating nuclear factor-E2-related factor2 (Nrf2), thereby inhibiting the proliferation, migration and inflammation of vascular cells, thereby exerting anti-inflammatory effects. The role of atherosclerosis.
5) Can effectively reduce portal hypertension: Endothelin-1 (ET-1) was used to induce portal hypertension in mice, and the effect of salvianolic acid B on blood microcirculation in the liver of mice with portal hypertension was investigated. , the results showed thatcompared with the control group,could significantly reduce the average blood flow and microcirculation flow rate in the liver of portal hypertension mice, and then play a role in reducing portal hypertension. Studies have shown that salvianolic acid B can reduce portal hypertension in rats, and studies have found that salvianolic acid B mainly acts through macrophages in the rat liver.