salvianolic acid b/نخر

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Salvianolic Acid B Down-regulates Matrix Metalloproteinase-9 Activity and Expression in Tumor Necrosis Factor-α-induced Human Coronary Artery Endothelial Cells.

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BACKGROUND Salvianolic acid B (Sal B) is a bioactive water-soluble compound of Salviae miltiorrhizae, a traditional herbal medicine that has been used clinically for the treatment of cardiovascular diseases. This study sought to evaluate the effect of Sal B on matrix metalloproteinase-9 (MMP-9) and

Salvianolic acid B from Salvia miltiorrhiza inhibits tumor necrosis factor-alpha (TNF-alpha)-induced MMP-2 upregulation in human aortic smooth muscle cells via suppression of NAD(P)H oxidase-derived reactive oxygen species.

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Activated matrix metalloproteinases (MMPs) in patients with acute coronary syndromes may contribute to plaque destabilization. Tumor necrosis factor-alpha (TNF-alpha) enhances NAD (P) H oxidase-dependent reactive oxygen species (ROS) formation and ROS induce MMP-2. In the present study, the effects

Salvianolic acid B attenuates VCAM-1 and ICAM-1 expression in TNF-alpha-treated human aortic endothelial cells.

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Attachment to, and migration of leukocytes into the vessel wall is an early event in atherogenesis. Expression of cell adhesion molecules by the arterial endothelium may play a major role in atherosclerosis. It has been suggested that antioxidants inhibit the expression of adhesion molecules and may

Study on the mechanisms of an extract of Salvia miltiorrhiza on the regulation of permeability of endothelial cells exposed to tumour necrosis factor-alpha.

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Exposure of endothelial cells to tumour necrosis factor-alpha (TNF-alpha) results in increased endothelial permeability, accompanied by a loss of cell-cell adherence junctions. The importance of tyrosine phosphatase and kinase activity in oxidant-mediated loss of cell junction structures has been

Effect of salvianolic acid B on TNF-α induced cerebral microcirculatory changes in a micro-invasive mouse model.

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OBJECTIVE To investigate the effects of salvianolic acid B (SAB) on tumor necrosis factor a (TNF-α) induced alterations of cerebral microcirculation with a bone-abrading model. METHODS The influences of craniotomy model and bone-abrading model on cerebral microcirculation were compared. The

Salvianolic Acid B Promotes the Survival of Random-Pattern Skin Flaps in Rats by Inducing Autophagy.

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Random-pattern skin flap transplantation is frequently applied in plastic and reconstructive surgery. However, the distal part of the flap often suffers necrosis due to ischemia. In this study, the effects of salvianolic acid B (Sal B) on flap survival were evaluated, and the underlying mechanisms

Salvianolic acid B attenuates plasminogen activator inhibitor type 1 production in TNF-alpha treated human umbilical vein endothelial cells.

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Plasminogen activator inhibitor type 1 (PAI-1), which plays a role in the development of atherosclerosis, is produced by endothelial cells following stimulation with various inflammatory cytokines such as tumor necrosis factor (TNF-alpha). In the present study, we investigated the effects of a

[Effect of salvianolic acid B on CD14 expression in rats with liver fibrosis].

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OBJECTIVE To observe the effect of salvianolic acid B (SAB), an extract from Radix Salviae miltiorrhizae, on expression of leucocyte differentiation antigen 14 (CD14) in the liver tissue of experimental rats with carbon tetrachloride (CCl4)-induced liver fibrosis. METHODS Thirty SD rats were

Combined Salvianolic Acid B and Ginsenoside Rg1 Exerts Cardioprotection against Ischemia/Reperfusion Injury in Rats.

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Lack of pharmacological strategies in clinics restricts the patient prognosis with myocardial ischemia/reperfusion (I/R) injury. The aim of this study was to evaluate the cardioprotection of combined salvianolic acid B (SalB) and ginsenoside Rg1 (Rg1) against myocardial I/R injury and further

Salvianolic acid B protects from pulmonary microcirculation disturbance induced by lipopolysaccharide in rat.

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The aim of the present study was to examine the effect and possible mechanism of salvianolic acid B (SalB) on pulmonary microcirculation disturbance induced by lipopolysaccharide (LPS) in rat. Male Sprague-Dawley rats were subjected to thoracotomy under continuous anesthesia and mechanical

Antagonism by salvianolic acid B of lipopolysaccharide-induced disseminated intravascular coagulation in rabbits.

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The aim of the present study was to investigate the effects of salvianolic acid B on lipopolysaccharide (LPS)-induced disseminated intravascular coagulation (DIC) in rabbits. Continuous infusion of LPS was used to induce a DIC model in rabbits. Treatment with salvianolic acid B (1, 3 or 6 mg/kg) was

Salvianolic acid B inhibits atherogenesis of vascular cells through induction of Nrf2-dependent heme oxygenase-1.

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OBJECTIVE Salvianolic acid B (Sal B), one of the most active components of Danshen extracts, has beneficial roles in the prevention and treatment of cardiovascular diseases. However, the precise mechanism by which Sal B exerts its effects on vascular cells is unclear. We aimed to elucidate the

Cardioprotective effect of salvianolic acid B against arsenic trioxide-induced injury in cardiac H9c2 cells via the PI3K/Akt signal pathway.

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The clinical use of arsenic trioxide (ATO), a potent anti-neoplastic agent, is often limited because of its severe cardiotoxicity. Salviae miltiorrhiza is widely used for the treatment of cardiovascular diseases. One of the most abundant ingredients of S. miltiorrhiza is salvianolic acid B (Sal B).

Protective effects and potential mechanism of salvianolic acid B on sodium laurate-induced thromboangiitis obliterans in rats.

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The root of Salvia miltiorrhiza f. alba (RSMA) (Lamiaceae) is used for the treatment of patients with thromboangiitis obliterans (TAO) in traditional Chinese medicine. Previously, a mixture of phenolic acids extracted from RSMA has shown significant protective effects on TAO

Salvianolic acid B inhibits the TLR4-NFκB-TNFα pathway and attenuates neonatal rat cardiomyocyte injury induced by lipopolysaccharide.

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OBJECTIVE To investigate the role of the TLR4-NFκB-TNFα inflammation pathway on: lipopolysaccharide (LPS)-induced neonatal rat cardiomyocyte injury and the possible protective effects of salvianolic acid B (Sal B). METHODS Wistar rat (1-2 days old) cardiomyocytes were isolated and cultured. Sal B

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