SalidrosideCAS# 10338-51-9 |
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| Cas No. | 10338-51-9 | SDF | Download SDF |
| PubChem ID | 159278 | Appearance | White powder |
| Formula | C14H20O7 | M.Wt | 300.30 |
| Type of Compound | Phenols | Storage | Desiccate at -20°C |
| Synonyms | Rhodioloside | ||
| Solubility | Soluble to 60 mg/mL (199.8 mM) in DMSO | ||
| Chemical Name | (2R,3S,4S,5R,6R)-2-(hydroxymethyl)-6-[2-(4-hydroxyphenyl)ethoxy]oxane-3,4,5-triol | ||
| SMILES | C1=CC(=CC=C1CCOC2C(C(C(C(O2)CO)O)O)O)O | ||
| Standard InChIKey | ILRCGYURZSFMEG-RKQHYHRCSA-N | ||
| Standard InChI | InChI=1S/C14H20O7/c15-7-10-11(17)12(18)13(19)14(21-10)20-6-5-8-1-3-9(16)4-2-8/h1-4,10-19H,5-7H2/t10-,11-,12+,13-,14-/m1/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Salidroside is a prolyl endopeptidase inhibitor, which has cardioprotective, antidiabetic,antidepressant, anxiolytic, anti-tumor, and antioxidant actions. Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activating mTOR signalling. It alleviates the pulmonary symptoms of paraquat-induced acute lung injury, at least partially, by repressing inflammatory cell infiltration and the expression of TGF-β1 resulting in delayed lung fibrosis; and it has protective effect against hypoxia-induced cardiomyocytes necrosis and apoptosis by increasing HIF-1α expression and subsequently up-regulating VEGF levels. It may be a potential therapeutic agent for treating or preventing neurodegenerative diseases implicated with oxidative stress. |
| Targets | VEGFR | JAK | STAT | MMP(e.g.TIMP) | PI3K | Akt | AMPK | GSK-3 | TNF-α | NF-kB | AP-1 | TGF-β/Smad | COX | NOS | Beta Amyloid |
| In vitro | Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway.[Pubmed: 25755753]Int J Clin Exp Pathol. 2015 Jan 1;8(1):615-21. eCollection 2015.Salidroside is considered to have anti-tumor properties. We investigate its effects on colon carcinoma SW1116 cells.
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| In vivo | Salidroside ameliorates insulin resistance through activation of a mitochondria-associated AMPK/PI3K/Akt/GSK3β pathway.[Pubmed: 25754463]Br J Pharmacol. 2015 Mar 5.Recent reports have suggested that Salidroside could protect cardiomyocytes from oxidative injury and stimulate glucose uptake in skeletal muscle cells by activating AMP-activated protein kinase (AMPK). The aim of this study was to evaluate the therapeutic effects of Salidroside on diabetic mice and to explore the underlying mechanisms.
Salidroside rescued mice from experimental sepsis through anti-inflammatory and anti-apoptosis effects.[Pubmed: 25676465]J Surg Res. 2015 Jan 14. pii: S0022-4804(15)00057-8.Salidroside (SDS) is the main effective component of Rhodiola rosea L with a variety of pharmacologic properties. The objective of this study was to investigate the efficacy of SDS in the treatment of experimental sepsis in mice and explore the possible underlying action mechanisms.
Salidroside attenuates beta amyloid-induced cognitive deficits via modulating oxidative stress and inflammatory mediators in rat hippocampus.[Pubmed: 23396166]Behav. Brain Res., 2013, 244(244):70–81.Beta amyloid (Aβ)-induced oxidative stress and chronic inflammation in the brain are considered to be responsible for the pathogenesis of Alzheimer's disease (AD). Salidroside, the major active ingredient of Rhodiola crenulata, has been previously shown to have antioxidant and neuroprotective properties in vitro. The present study aimed to investigate the protective effects of Salidroside on Aβ-induced cognitive impairment in vivo.
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| Animal Research | Salidroside alleviates paraquat-induced rat acute lung injury by repressing TGF-β1 expression.[Pubmed: 25674253]Effects of Salidroside on Myocardial Injury In Vivo In Vitro via Regulation of Nox/NF-κB/AP1 Pathway.[Pubmed: 25682470]Inflammation. 2015 Feb 15.Animal Models: Male Sprague-Dawley rats Int J Clin Exp Pathol. 2014 Dec 1;7(12):8841-7. eCollection 2014.Animal Models: Male rats (190-210 g) |
Salidroside Dilution Calculator
Salidroside Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.33 mL | 16.65 mL | 33.3 mL | 66.6001 mL | 83.2501 mL |
| 5 mM | 0.666 mL | 3.33 mL | 6.66 mL | 13.32 mL | 16.65 mL |
| 10 mM | 0.333 mL | 1.665 mL | 3.33 mL | 6.66 mL | 8.325 mL |
| 50 mM | 0.0666 mL | 0.333 mL | 0.666 mL | 1.332 mL | 1.665 mL |
| 100 mM | 0.0333 mL | 0.1665 mL | 0.333 mL | 0.666 mL | 0.8325 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Salidroside is a prolyl endopeptidase Inhibitor. Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activating mTOR signalling.
In Vitro:Salidroside (100 μM) inhibits prolyl endopeptidase (PEP) activity (10.6±1.9%). Prolyl endopeptidase is an enzyme that plays a role in the metabolism of proline-containing neuropeptidase which is recognized to be involved in learning and memory[1]. Salidroside, one of the major phenylpropanoid glycosides found in R. rosea L, is consumed almost daily as a nutritional supplement in many countries and has been identified possessing potential anti-fatigue and anoxia,anti-aging, and anti-Alzheimer's disease activities. Salidroside can improve muscle nutrition via increasing mTOR, p-mTOR, and MyHC expression[2]. SH-SY5Y cells are exposed to 0-600 μM MPP+ for 12-48 h and the results show that MPP+ results in a significant decrease of cell viability in a concentration and time-dependent manner. Cells are pretreated with 25-100 μM Salidroside (Sal) for 24 h and then exposed to 500 μM MPP+ for an additional 24 h. Salidroside concentration-dependently prevents MPP+-induced decrease of cell viability. Annexin V/PI staining is a common method for the detection of apoptotic cell. Salidroside significantly decreases the number of Annexin V/PI-stained cells treated by MPP+ which is in a concentration-dependent manner. Apoptotic cell could also be morphologically evaluated by Hoechst staining. In Hoechst staining, apoptotic cells are characterized by reduced nuclear size, chromatin condensation, intense fluorescence, and nuclear fragmentation. Salidroside notably inhibits MPP+-induced increase of chromatin condensation, intense fluorescence, and nuclear fragmentation in SH-SY5Y cells[3]
In Vivo:Salidroside is a natural antioxidant extracted from medicinal food plant Rhodiola rosea. Salidroside (100 mg/kg/day) shows strong glucose lowering effect on db/db mice which is similar to effect of Metformin (200 mg/kg/day). For this reason, the dose of 100 mg/kg/day salidroside is used[4].
References:
[1]. Fan W, et al. Prolyl endopeptidase inhibitors from the underground part of Rhodiola sachalinensis. Chem Pharm Bull (Tokyo). 2001 Apr;49(4):396-401.
[2]. Chen X, et al. Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activatingmTOR signalling. J Cachexia Sarcopenia Muscle. 2016 May;7(2):225-32.
[3]. Wu L, et al. Salidroside Protects against MPP+-Induced Neuronal Injury through DJ-1-Nrf2 Antioxidant Pathway. Evid Based Complement Alternat Med. 2017;2017:5398542.
[4]. Ju L, et al. Salidroside, A Natural Antioxidant, Improves β-Cell Survival and Function via Activating AMPK Pathway. Front Pharmacol. 2017 Oct 18;8:749.
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Salidroside attenuates beta amyloid-induced cognitive deficits via modulating oxidative stress and inflammatory mediators in rat hippocampus.[Pubmed:23396166]
Behav Brain Res. 2013 May 1;244:70-81.
Beta amyloid (Abeta)-induced oxidative stress and chronic inflammation in the brain are considered to be responsible for the pathogenesis of Alzheimer's disease (AD). Salidroside, the major active ingredient of Rhodiola crenulata, has been previously shown to have antioxidant and neuroprotective properties in vitro. The present study aimed to investigate the protective effects of Salidroside on Abeta-induced cognitive impairment in vivo. Rats received intrahippocampal Abeta1-40 injection were treated with Salidroside (25, 50 and 75 mg/kg p.o.) once daily for 21 days. Learning and memory performance were assessed in the Morris water maze (days 17-21). After behavioral testing, the rats were sacrificed and hippocampi were removed for biochemical assays (reactive oxygen species (ROS), superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA), acetylcholinesterase (AChE), acetylcholine (ACh)) and molecular biological analysis (Cu/Zn-SOD, Mn-SOD, GPx, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, nuclear factor kappaB (NF-kappaB), inhibitor of kappaB-alpha (IkappaBalpha), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), receptor for advanced glycation end products (RAGE)). Our results confirmed that Abeta1-40 peptide caused learning and memory deficits in rats. Further analysis demonstrated that the NADPH oxidase-mediated oxidative stress was increased in Abeta1-40-injected rats. Furthermore, NF-kappaB was demonstrated to be activated in Abeta1-40-injected rats, and the COX-2, iNOS and RAGE expression were also induced by Abeta1-40. However, Salidroside (50 and 75 mg/kg p.o.) reversed all the former alterations. Thus, the study indicates that Salidroside may have a protective effect against AD via modulating oxidative stress and inflammatory mediators.
Salidroside ameliorates insulin resistance through activation of a mitochondria-associated AMPK/PI3K/Akt/GSK3beta pathway.[Pubmed:25754463]
Br J Pharmacol. 2015 Jul;172(13):3284-301.
BACKGROUND AND PURPOSE: Recent reports have suggested that Salidroside could protect cardiomyocytes from oxidative injury and stimulate glucose uptake in skeletal muscle cells by activating AMP-activated protein kinase (AMPK). The aim of this study was to evaluate the therapeutic effects of Salidroside on diabetic mice and to explore the underlying mechanisms. EXPERIMENTAL APPROACH: The therapeutic effects of Salidroside on type 2 diabetes were investigated. Increasing doses of Salidroside (25, 50 and 100 mg.kg(-1) .day(-1)) were administered p.o. to db/db mice for 8 weeks. Biochemical analysis and histopathological examinations were conducted to evaluate the therapeutic effects of Salidroside. Primary cultured mouse hepatocytes were used to further explore the underlying mechanisms in vitro. KEY RESULTS: Salidroside dramatically reduced blood glucose and serum insulin levels and alleviated insulin resistance. Hypolipidaemic effects and amelioration of liver steatosis were observed after Salidroside administration. In vitro, Salidroside dose-dependently induced an increase in the phosphorylations of AMPK and PI3K/Akt, as well as glycogen synthase kinase 3beta (GSK3beta) in hepatocytes. Furthermore, Salidroside-stimulated AMPK activation was found to suppress the expression of PEPCK and glucose-6-phosphatase. Salidroside-induced AMPK activation also resulted in phosphorylation of acetyl CoA carboxylase, which can reduce lipid accumulation in peripheral tissues. In isolated mitochondria, Salidroside inhibited respiratory chain complex I and disturbed oxidation/phosphorylation coupling and moderately depolarized the mitochondrial membrane potential, resulting in a transient increase in the AMP/ATP ratio. CONCLUSIONS AND IMPLICATIONS: Salidroside exerts an antidiabetic effect by improving the cellular metabolic flux through the activation of a mitochondria-related AMPK/PI3K/Akt/GSK3beta pathway.
Effects of Salidroside on Myocardial Injury In Vivo In Vitro via Regulation of Nox/NF-kappaB/AP1 Pathway.[Pubmed:25682470]
Inflammation. 2015 Aug;38(4):1589-98.
Salidroside (Sal), a phenylpropanoid glycoside isolated from a popular traditional Chinese medicinal plant Rhodiola rosea L., possesses multiple pharmacological actions. This aim of this study is to investigate the effects of Sal against isoproterenol (ISO)-induced myocardial ischemia. Fifty male Sprague-Dawley rats were randomized equally to five groups: control group, ISO group, Sal (20 mg/kg; 40 mg/kg) treatments groups, and propranolol (Pro, 15 mg/kg) group. Rats were treated for 14 days and then given ISO (80 mg/kg) for 2 consecutive days by subcutaneous injection. In vitro, we used H9C2 cells to investigate the effects of Sal against hypoxia-reoxygenation. ST-segment elevation was measured after the last administration. Serum levels of creatine kinase (CK), lactate dehydrogenase (LDH), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), superoxide dismutase (SOD), and malondialdehyde (MDA); levels of NADPH oxidases 2 and 4 (Nox2 and Nox4), NF-kappaBP65, and AP1 in heart, and H9C2 cells were measured by Western blot. The hearts were excised for determining microscopic examination, SOD, and MDA measurements. Sal decreased the ST elevation induced by ISO, decreased serum levels of CK-MB, LDH, TNF-alpha, IL-6, SOD, and MDA. In addition, Sal increased SOD activity and decreased MDA content in myocardial tissue. Sal also decreased Nox2 and 4, NF-kappaBP65, P-NF-kappaBP65, and AP1 protein levels in the heart. The results support a further study of Sal as potential treatments for ischemic heart disease.
Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway.[Pubmed:25755753]
Int J Clin Exp Pathol. 2015 Jan 1;8(1):615-21. eCollection 2015.
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. Western blot was used to detect the expression of STAT3 signal related proteins. As the result, high concentrations of Salidroside (10, 20. 50 mug/ml) significantly inhibited proliferation of SW1116 cells in a parallelly, cell cycle arrest was increased at the G0/G1 phase after Salidroside treatment. Furthermore, Salidroside inhibited migration and invasion of SW1116 cells. Salidroside treatment decreased proteins expression of phosphorylation levels in JAK2/STAT3 signaling, while MMP-2 and MMP-9 proteins levels were decreased and protein expression of VEGF and VEGFR-2 were down-regulated. In Conclusion, Salidroside inhibited proliferation, decreased the migration and invasion of SW1116 cells in JAK2/STAT3-dependent pathway, the specific mechanisms need further study.
