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salidroside/nekros
Länken sparas på Urklipp
Sida 1 från 51 resultat
Salidroside prevents tumor necrosis factor-α-induced vascular inflammation by blocking mitogen-activated protein kinase and NF-κB signaling activation.
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Vascular inflammation is a key factor in the pathogenesis of atherosclerosis. Salidroside is an important active ingredient extracted from the root of the Rhodiola rosea plant, which has been reported to have antioxidative, anti-cancer, neuroprotective and cardioprotective effects. However,
Salidroside inhibits oxygen glucose deprivation (OGD)/re-oxygenation-induced H9c2 cell necrosis through activating of Akt-Nrf2 signaling.
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Oxygen glucose deprivation (OGD)/re-oxygenation has been applied to cultured cardiomyocytes to create a cellular model of ischemic heart damage. In the current study, we explored the potential role of salidroside against OGD/re-oxygenation-induced damage in H9c2 cardiomyocytes, and studied the
Effects of salidroside pretreatment on expression of tumor necrosis factor-alpha and permeability of blood brain barrier in rat model of focal cerebralischemia-reperfusion injury.
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OBJECTIVE
To observe changes in expression of tumor necrosis factor (TNF)-alpha and permeability of blood brain barrier after salidroside pretreatment in rats with injury induced by focal cerebralischemia-reperfusion.
METHODS
Forty-five male SD rats were randomly divided into three groups (n=15):
Salidroside inhibits steroid-induced avascular necrosis of the femoral head via the PI3K/Akt signaling pathway: In vitro and in vivo studies.
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Dexamethasone (Dex) and other glucocorticoids are widely used to treat serious infections and immunological diseases, however they may cause steroid‑induced avascular necrosis of the femoral head (SANFH). Salidroside (Sal) has demonstrated an anti‑apoptotic effect on neurocytes by activating the
Salidroside Protects Lipopolysaccharide-Induced Acute Lung Injury in Mice.
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Salidroside (SDS) has been reported to have anti-inflammatory properties. The objective of this study was to investigate the protective effect of SDS on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. BALB/c mice were pretreated with SDS 1 hour before intranasal instillation of
Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activating mTOR signalling.
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BACKGROUND
Cachexia has a devastating impact on survival and quality of life for many cancer patients and contributes to nearly one-third of all cancer deaths; also, it is associated with poor responses to chemotherapy and survival. A better understanding of the underlying mechanisms of
Salidroside protects against hydrogen peroxide-induced injury in cardiac H9c2 cells via PI3K-Akt dependent pathway.
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Oxidative stress induces serious tissue injury in cardiovascular diseases. Salidroside, with its strong antioxidative and cytoprotective actions, is of particular interest in the development of antioxidative therapies for oxidative injury in cardiac diseases. We examined the pharmacological effects
Salidroside suppresses solar ultraviolet-induced skin inflammation by targeting cyclooxygenase-2.
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Solar ultraviolet (SUV) irradiation causes skin disorders such as inflammation, photoaging, and carcinogenesis. Cyclooxygenase-2 (COX-2) plays a key role in SUV-induced skin inflammation, and targeting COX-2 may be a strategy to prevent skin disorders. In this study, we found that the expression of
Salidroside Inhibits Lipopolysaccharide-ethanol-induced Activation of Proinflammatory Macrophages via Notch Signaling Pathway.
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Activation of macrophages is a key event for the pathogenesis of various inflammatory diseases. Notch signaling pathway recently has been found to be a critical pathway in the activation of proinflammatory macrophages. Salidroside (Sal), one of main bioactive components in Rhodiola crenulata (Hook.
Hepatoprotective effects of salidroside on fulminant hepatic failure induced by D-galactosamine and lipopolysaccharide in mice.
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OBJECTIVE
The aim was to investigate the protective effect of salidroside isolated from Rhodiola sachalinensis A. Bor. (Crassulaceae) on D-galactosamine/lipopolysaccharide-induced fulminant hepatic failure.
METHODS
Hepatotoxicity was induced by an intraperitoneal injection of D-galactosamine (700
Salidroside attenuates LPS-stimulated activation of THP-1 cell-derived macrophages through down-regulation of MAPK/NF-kB signaling pathways.
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Excessive activation of macrophages is implicated in various inflammatory injuries. Salidroside (Sal), one of the main bioactive components of Rhodiola Sachalinensis, has been reported to possess anti-inflammatory activities. This study aimed to examine the effect of Sal on the activation of
Protective effects of salidroside against acetaminophen-induced toxicity in mice.
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The protective effect of salidroside (SDS) isolated from Rhodiola sachalinensis A. BOR. (Crassulaceae), was investigated in acetaminophen (APAP)-induced hepatic toxicity mouse model in comparison to N-acetylcysteine (NAC). Drug-induced hepatotoxicity was induced by an intraperitoneal (i.p.)
[Protective effects of salidroside on injury induced by hypoxia/hypoglycemia in cultured neurons].
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OBJECTIVE
To study the protective effects of salidroside on injury induced by hypoxia/hypoglycemia in cultured SH-SY5Y cell.
METHODS
Apoptosis and intracellular free calcium concentration ([Ca2+]i) were measured by flow cytometry, morphological changes and neuronal necrosis were observed with
Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats.
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Successful drug treatment for sepsis-related acute lung injury (ALI) remains a major clinical problem. Thus, the aim of the present study was to investigate the beneficial effects of salidroside on ameliorating cecal ligation and puncture (CLP)-induced lung inflammation. Rats underwent CLP surgery
[Effects of salidroside on the secretion of inflammatory mediators induced by lipopolysaccharide in the co-culture of rat alveolar macrophages and type II alveolar epithelial cells].
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The aim of the present study was to investigate the effect of salidroside (Sal) on inflammatory activation induced by lipopolysaccharide (LPS) in the co-culture of rat alveolar macrophages (AM) NR 8383 and type II alveolar epithelial cells (AEC II) RLE-6TN. CCK-8 colorimetric method was used to
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