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salidroside/inflammation
Врската е зачувана во таблата со исечоци
Страница 1 од 134 резултати
Salidroside-Mitigated Inflammatory Injury of Hepatocytes with Non-Alcoholic Fatty Liver Disease via Inhibition TRPM2 Ion Channel Activation.
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Salidroside improves glucose homeostasis in obese mice by repressing inflammation in white adipose tissues and improving leptin sensitivity in hypothalamus.
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Salidroside is a functionally versatile natural compound from the perennial flowering plant Rhodiola rosea L. Here, we examined obese mice treated with salidroside at the dosage of 50 mg/kg/day for 48 days. Mice treated with salidroside showed slightly decreased food intake, body weight and hepatic
Antidepressant-like effects of salidroside on olfactory bulbectomy-induced pro-inflammatory cytokine production and hyperactivity of HPA axis in rats.
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Salidroside (SA) is the primary bioactive marker compound in the standardized extracts from Rhodiola rosea. Although it has potential antidepressant activity in a rat behavioral despair model, the mechanisms of antidepressant effect for SA remain unclear. The objective of this study was to evaluate
Salidroside attenuates endothelial cellular senescence via decreasing the expression of inflammatory cytokines and increasing the expression of SIRT3.
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Endothelial cellular senescence is an important contributor to the endothelial dysfunction and atherosclerosis. Our previous studies suggested that salidroside (SAL) can alleviate atherosclerosis and protect endothelial cells against oxidative stress induced damage. However, the effect and mechanism
Salidroside protected against MPP+ -induced Parkinson's disease in PC12 cells by inhibiting inflammation, oxidative stress and cell apoptosis.
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The present study aimed to investigate the protective effects of salidroside (SAL) on 1-methyl-4-phenylpyridinium (MPP+ )-induced PC12 cell model for Parkinson's disease. PC12 cells were pretreated with SAL in different concentrations and then exposed to MPP+ . To evaluate the
[Effects of salidroside on the secretion of inflammatory mediators induced by lipopolysaccharide in murine macrophage cell line J774.1].
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To investigate the effect of salidroside (Sal) on the inflammatory activation of lipopolysaccharide (LPS)-induced murine macrophage cell line J774.1 and its possible mechanism, the cells were treated with PBS, LPS (0.5 µg/mL) or different doses of Sal (5, 25, 125 µg/mL) + LPS (0.5 µg/mL). CCK-8
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 attenuates interleukin-1β-induced inflammation in human osteoarthritis chondrocytes.
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Salidroside, a bioactive constituent isolated from Rhodiola rosea, has been reported to have anti-inflammatory effects. However, the effects of salidroside on interleukin (IL)-1β-stimulated osteoarthritis (OA) chondrocytes remain to be elucidated. Thus, this study aimed to evaluate the
Salidroside attenuates allergic airway inflammation through negative regulation of nuclear factor-kappa B and p38 mitogen-activated protein kinase.
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Salidroside is a biologically active ingredient of Rhodiola rosea, which has several interesting biological properties, including anti-oxidant and anti-inflammatory; however, its anti-allergic effects are poorly understood. The objective of this study is to determine whether salidroside attenuates
[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
Salidroside Regulates Inflammatory Response in Raw 264.7 Macrophages via TLR4/TAK1 and Ameliorates Inflammation in Alcohol Binge Drinking-Induced Liver Injury.
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The current study was designed to investigate the anti-inflammatory effect of salidroside (SDS) and the underlying mechanism by using lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages in vitro and a mouse model of binge drinking-induced liver injury in vivo. SDS downregulated protein
Salidroside can target both P4HB-mediated inflammation and melanogenesis of the skin
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Rationale: Many external factors can induce the melanogenesis and inflammation of the skin. Salidroside (SAL) is the main active ingredient of Rhodiola, which is a perennial grass plant of the Family Crassulaceae. This study evaluated the effect and molecular mechanism of SAL on skin
Anti-inflammatory effect of salidroside on phorbol-12-myristate-13-acetate plus A23187-mediated inflammation in HMC-1 cells.
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Salidroside [2-(4-hydroxyphenyl)ethyl β-D-gluco-pyranoside (SAS)] has been identified as the most potent ingredient of the plant Rhodiola rosea L. Previous studies have demonstrated that it possesses a number of pharmacological properties, including anti-aging, anti-fatigue, antioxidant, anticancer
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 Restores an Anti-inflammatory Endothelial Phenotype by Selectively Inhibiting Endothelial Complement After Oxidative Stress.
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Salidroside, an active component of Rhodiola rosea, reduces inflammation and neuronal damage after middle cerebral artery occlusion (MCAO) with reperfusion, partly by inhibiting cerebral complement C3 activation. However, the mechanisms of this inhibition are not fully understood. In this study, we
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