salidroside/neoplasms

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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

Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway.

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Salidroside is considered to have anti-tumor properties. We investigate its effects on colon carcinoma SW1116 cells. Cell viability was assessed by CCK-8. Propidium iodide (PI) staining was used to determine the cell cycle by flow cytometry. The migration and invasion were detected by Transwell.

[Salidroside induces anti-tumor effect in dendritic cells via ERK pathway].

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Objective To investigate the role of mitogen activated protein kinase/extracellular signal-regulated kinase (MAPK/ERK) pathway in the salidroside (SAL)-regulated antitumor immunity of dendritic cells (DCs). Methods Lewis lung cancer-bearing mouse model was established and treated with normal saline

Salidroside inhibits proliferation, migration and invasion of human pancreatic cancer PANC1 and SW1990 cells through the AKT and ERK signaling pathway

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Salidroside is the main compounds extracted from the Chinese medicine Rhodiola rosea and has many pharmacological effects, including anti-tumor effects. However, the role of salidroside in human pancreatic cancer remains poorly known. Thus, the focus of this study was to evaluate the

The influence of Rhodiola quadrifida 50% hydro-alcoholic extract and salidroside on tumor-induced angiogenesis in mice.

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The genus Rhodiola (Crassulaceae) consists of more than 100 species. They grow mainly in Tibet, China and Mongolia and are traditionally used as tonic, adaptogen, antidepressant and anti-inflammatory drugs. The best known is Rhodiola rosea (R. rosea) now cultivated also in Europe and North America,

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,

Enhancing the chemotherapy effect of Apatinib on gastric cancer by co-treating with salidroside to reprogram the tumor hypoxia micro-environment and induce cell apoptosis.

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Hypoxic microenvironment commonly occurred in the solid tumors considerably decreases the chemosensitivity of cancer cells. Salidroside (Sal), the main active ingredient of Rhodiola rosea, was shown to be able of regulating the tumor hypoxia micro-environment and enhancing the

Anticancer effect of salidroside reduces viability through autophagy/PI3K/Akt and MMP-9 signaling pathways in human bladder cancer cells.

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Salidroside has a wide range of pharmacological activities, including antitumor, anti-inflammatory, analgesic, antibacterial, antiviral and anti-fertility abilities. In the present study, the effects of salidroside on the viability and apoptosis of bladder cancer cells, and the potential underlying

Development of lipid-shell and polymer core nanoparticles with water-soluble salidroside for anti-cancer therapy.

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Salidroside (Sal) is a potent antitumor drug with high water-solubility. The clinic application of Sal in cancer therapy has been significantly restricted by poor oral absorption and low tumor cell uptake. To solve this problem, lipid-shell and polymer-core nanoparticles (Sal-LPNPs) loaded with Sal

Effects of salidroside on glioma formation and growth inhibition together with improvement of tumor microenvironment.

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OBJECTIVE To test the effects of salidroside on formation and growth of glioma together with tumor microenvironment. METHODS Salidroside extracted from Rhodiola rosea was purified and treated on human glioma cells U251 at the concentration of 20 µg/mL.

Salidroside induces apoptosis and protective autophagy in human gastric cancer AGS cells through the PI3K/Akt/mTOR pathway.

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Salidroside, a natural active ingredient extracted from Rhodiola rosea, has been shown to exert antitumor activity against breast cancer Dong Young et al. [1], colon cancer Sun et al. [2] and bladder cancer Tian et al. [3]. However, the effect of salidroside on apoptosis and autophagy in gastric

Salidroside suppresses nonsmall cell lung cancer cells proliferation and migration via microRNA-103-3p/Mzb1.

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Lung cancer is the leading cause of cancer death in both men and women in the worldwide. Metastasis is the leading cause of cancer mortality and is a major hurdle for lung cancer treatment. Salidroside, a glycoside of tyrosol, is isolated from Rhodiola rosea and shows anticancer functions in several

Anticancer effect of salidroside on A549 lung cancer cells through inhibition of oxidative stress and phospho-p38 expression.

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Oxidative stress is important in carcinogenesis and metastasis. Salidroside, a phenylpropanoid glycoside isolated from Rhodiola rosea L., shows potent antioxidant properties. The aim of the present study was to investigate the roles of salidroside in cell proliferation, the cell cycle, apoptosis,

Salidroside induces cell-cycle arrest and apoptosis in human breast cancer cells.

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Recently, salidroside (p-hydroxyphenethyl-beta-d-glucoside) has been identified as one of the most potent compounds isolated from plants of the Rhodiola genus used widely in traditional Chinese medicine, but pharmacokinetic data on the compound are unavailable. We were the first to report the

Salidroside inhibits the growth of human breast cancer in vitro and in vivo.

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Salidroside has been identified as one of the most potent compounds isolated from the plant Rhodiola rosea, and was found to have several important biological properties, including antioxidant and anti-inflammatory activity; however, its anticancer effects are poorly understood. Thus, the present

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