Product name: Salidroside
Synonym name: Rhodosin; Rhodioloside
Catalogue No.: BP1246
Cas No.: 10338-51-9
Formula: C14H20O7
Mol Weight: 300.307
Botanical Source: Rhodiolae Crenulatae Radixet Rhizoma
Physical Description:
Type of Compound: Phenols
Purity: 95%~99%
Analysis Method: HPLC-DAD or/and HPLC-ELSD
Identification Method: Mass, NMR
Packing: Brown vial or HDPE plastic bottle
Storage: Store in a well closed container, protected from air and light. Put into refrigerate or freeze for long term storage.
Whenever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20℃. Generally, these will be useable for up to two weeks.
The product could be supplied from milligrams to grams
Inquire for bulk scale.
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.
References:
Int J Clin Exp Pathol. 2015 Jan 1;8(1):615-21. eCollection 2015.
Anticancer effect of salidroside on colon cancer through inhibiting JAK2/STAT3 signaling pathway.
Salidroside is considered to have anti-tumor properties. We investigate its effects on colon carcinoma SW1116 cells.
METHODS AND RESULTS:
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 μg/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.
CONCLUSIONS:
In Conclusion, Salidroside inhibited proliferation, decreased the migration and invasion of SW1116 cells in JAK2/STAT3-dependent pathway, the specific mechanisms need further study.
Br J Pharmacol. 2015 Mar 5.
Salidroside ameliorates insulin resistance through activation of a mitochondria-associated AMPK/PI3K/Akt/GSK3β pathway.
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.
METHODS AND RESULTS:
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. 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 3β (GSK3β) 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:
Salidroside exerts an antidiabetic effect by improving the cellular metabolic flux through the activation of a mitochondria-related AMPK/PI3K/Akt/GSK3β pathway.
J Surg Res. 2015 Jan 14. pii: S0022-4804(15)00057-8.
Salidroside rescued mice from experimental sepsis through anti-inflammatory and anti-apoptosis effects.
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.
METHODS AND RESULTS:
Sepsis was induced in C57BL/6 male mice via cecal ligation and puncture (CLP). The animals were divided into three groups as follows: sham, CLP, and CLP plus SDS. SDS (50 mg/kg) was injected intraperitoneally 1 h after operation. Postoperative survival of the mice, bacterial clearance in blood and peritoneal lavage fluid, cytokine secretion in blood, and histology of lung were evaluated. In addition, apoptosis of immune cells in the spleen and thymus were examined, respectively. SDS administration prolonged the survival of the septic mice, inhibited the proinflammatory responses, and enhanced bacterial clearance. It also alleviated the pathologic changes in the lung and inhibited the apoptosis of immune cells in the spleen and thymus after CLP challenge.
CONCLUSIONS:
SDS exerts a protective effect in CLP-induced sepsis by attenuating the proinflammatory responses, enhancing bacterial clearance, and preserving adaptive immunity. SDS may be a promising therapeutic strategy for the treatment of sepsis.
Behav. Brain Res., 2013, 244(244):70–81.
Salidroside attenuates beta amyloid-induced cognitive deficits via modulating oxidative stress and inflammatory mediators in rat hippocampus.
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 Salidrosideon Aβ-induced cognitive impairment in vivo.
METHODS AND RESULTS:
Rats received intrahippocampal Aβ1-40 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 κB (NF-κB), inhibitor of κB-alpha (IκBα), cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), receptor for advanced glycation end products (RAGE)). Our results confirmed that Aβ1-40 peptide caused learning and memory deficits in rats. Further analysis demonstrated that the NADPH oxidase-mediated oxidative stress was increased in Aβ1-40-injected rats. Furthermore, NF-κB was demonstrated to be activated in Aβ1-40-injected rats, and the COX-2, iNOS and RAGE expression were also induced by Aβ1-40. However, Salidroside (50 and 75 mg/kg p.o.) reversed all the former alterations.
CONCLUSIONS:
Thus, the study indicates that Salidroside may have a protective effect against AD via modulating oxidative stress and inflammatory mediators.
HPLC of Salidroside
HNMR of Salidroside
Storage conditions：Short-term storage at 2~8℃, long-term storage at -20 ~ -80℃
Salidroside (CAS number: 10338-51-9) is an active natural product isolated from plants of the Sedum genus, belonging to the glycoside class of compounds. As one of the main bioactive components in Rhodiola rosea, salidroside has attracted much attention due to its diverse pharmacological activities, especially showing significant potential in anti fatigue, neuroprotection, anti-tumor, and metabolic regulation. In recent years, with the in-depth study of its molecular mechanism, the role of salidroside in regulating cellular energy metabolism, mitochondrial function, and signal transduction pathways has gradually become clear, demonstrating its unique value as a novel natural medicine molecule.
This article provides a systematic review of the chemical structure and physicochemical properties, plant sources, and extraction methods of salidroside, with a focus on its pharmacological activity and mechanism of action. Combined with the latest molecular target research, it explores its pharmacological properties and pharmacokinetic characteristics. Finally, it looks forward to the prospects and challenges of its clinical application, aiming to provide a comprehensive theoretical basis and research reference for the field of natural product pharmacology and new drug development.
The chemical name of salidroside is 4- (β - D-glucopyranosyl) phenylethanol, with a molecular formula of C14H20O7 and a molecular weight of 300.3070. Its structure consists of a phenylethanol group connected to a glucose molecule through a β - glycosidic bond, belonging to the glycoside class of compounds. The LogP value of salidroside is -0.4086, indicating its strong hydrophilicity and good water solubility of 9.0354, which is beneficial for its absorption and distribution in vivo.
The polar surface area (TPSA) of salidroside is 119.6100 Å ², indicating its high polarity and the number of hydrogen bond donors/acceptors, which affects its ability to pass through cell membranes. Its blood-brain barrier permeability is low, indicating that the distribution of salidroside in the central nervous system is limited, but it can still exert neuroprotective effects by regulating the peripheral nervous system and indirect mechanisms. The hERG channel inhibition test result was negative, indicating that salidroside has a low risk of cardiac toxicity. The Ames mutagenicity test result was 0.0, indicating no significant genotoxicity.
Rhodiola rosea glycoside is mainly found in plants of the Rhodiola genus, with the highest content found in the rhizomes of Rhodiola rosea. Rhodiola rosea is a perennial herbaceous plant widely distributed in high-altitude and temperate regions, with a long history of medicinal use. Its rhizome contains abundant glycosides, phenols, and volatile oil components, among which salidroside is the most representative active ingredient.
There are various methods for extracting salidroside, with traditional methods using water extraction or ethanol extraction, combined with ultrasound assisted extraction technology to improve extraction efficiency. The common steps include: crushing the dried rhizomes of Rhodiola rosea, using a 50% -70% ethanol aqueous solution for reflux extraction, followed by filtration concentration, precipitation, and column chromatography purification to obtain high-purity salidroside. In recent years, supercritical CO2 extraction and membrane separation technologies have also been introduced to achieve green and efficient extraction processes.
Rhodiola rosea glycoside exhibits significant effects in various biological activities, including anti fatigue, neuroprotection, anti-tumor, and metabolic regulation.
anti-fatigue effect
Rhodiola rosea glycoside can significantly improve the body's endurance and anti fatigue ability. Animal experiments have shown that salidroside promotes fatty acid oxidation and mitochondrial function by regulating energy metabolism related targets such as AMPK, SIRT1, and PPARG, thereby delaying the occurrence of fatigue. In addition, salidroside also affects the neurotransmitter system, regulating targets such as MAOA, SLC6A4, ADRB2, and HTR1A, improving central nervous system function, enhancing mental state, and cognitive ability.
Neuroprotective effect
Rhodiola rosea glycoside enhances PINK1/Parkin mediated mitochondrial autophagy, protecting dopaminergic neurons from oxidative stress and apoptosis damage, demonstrating potential therapeutic value for neurodegenerative diseases such as Parkinson's disease. In addition, its antioxidant and anti-inflammatory effects also help alleviate nerve damage and promote nerve repair.
Anti tumor and alleviation of cachexia
Rhodiola rosea glycoside, as a prolyl endopeptidase (PEP) inhibitor, can alleviate cachexia symptoms in a mouse model of tumor cachexia by activating the mTOR signaling pathway, improving weight loss and muscle atrophy. Its ability to regulate cellular metabolism and immune microenvironment provides new ideas for adjuvant therapy of tumors.
Other pharmacological effects
Rhodiola rosea glycoside also exhibits multiple activities such as anti-inflammatory, antioxidant, cardiovascular protection, and immune regulation, involving multiple signaling pathways and molecular targets, demonstrating its broad pharmacological potential.
The multi-target mechanism of action of salidroside is the basis for its diverse pharmacological activities. It mainly involves the following key targets and signaling pathways:
AMPK（5' AMP-activated protein kinase）
As a key regulatory factor of cellular energy metabolism, the activation of AMPK promotes fatty acid oxidation and glucose metabolism. Rhodiola rosea improves energy metabolism imbalance and enhances the body's anti fatigue ability by activating AMPK.
SIRT1 (silencing information regulatory factor 2 related enzyme 1)
SIRT1 is involved in regulating cellular stress response and metabolic homeostasis, while salidroside promotes mitochondrial biogenesis and antioxidant response by activating SIRT1, protecting neuronal function.
PPARG (Peroxisome proliferator activated receptor gamma)
PPARG regulates lipid metabolism and inflammatory response, and salidroside improves lipid metabolism disorders and inflammatory states by regulating PPARG expression.
PINK1/Parkin mediated mitochondrial autophagy
Rhodiola rosea glycoside enhances the PINK1/Parkin signaling pathway, promotes the clearance of damaged mitochondria, maintains mitochondrial quality control, and protects dopaminergic neurons from damage.
MTOR signaling pathway
Rhodiola rosea glycoside activates mTOR signaling, regulates protein synthesis and cellular metabolism, and alleviates muscle atrophy and weight loss associated with tumor cachexia.
Neurotransmitter related targets
Rhodiola rosea glycoside regulates targets such as MAOA (monoamine oxidase A), SLC6A4 (serotonin transporter), ADRB2 (β 2 adrenergic receptor), HTR1A (serotonin receptor 1A), etc., improves neurotransmitter balance, and enhances central nervous system function.
UCP1 (uncoupling protein 1) and CREB1/BDNF signaling
Rhodiola rosea glycoside promotes thermogenesis and energy expenditure by regulating UCP1, activating CREB1 and BDNF signaling, and promoting neuroplasticity and cognitive function.
The pharmacological evaluation of salidroside shows that it has good safety and pharmacological potential. It has a moderate molecular weight (300.3070) and good water solubility (9.0354), which is beneficial for oral absorption. The LogP value is -0.4086, indicating its strong hydrophilicity, which may limit its cell membrane permeability but contribute to its solubility in blood circulation.
The low blood-brain barrier permeability suggests that salidroside has limited direct effects on the central nervous system, but it can still exert neuroprotective effects through regulating peripheral nerves and indirect mechanisms. The hERG inhibition test result is negative, indicating a low risk of cardiac toxicity. The Ames test is non mutagenic and has high safety.
Pharmacokinetic studies have shown that salidroside is rapidly absorbed in the body after oral administration, with a moderate plasma half-life. It is mainly metabolized by the liver and excreted by the kidneys. Its metabolites are mostly in the form of deglycosylation, and some have biological activity. The bioavailability of salidroside is affected by intestinal enzymatic hydrolysis and first pass effects. In the future, through formulation improvement and optimized administration routes, its clinical application value is expected to be enhanced.
Rhodiola glycoside, as a multifunctional natural product, has broad clinical application potential. Its anti fatigue effect is suitable for auxiliary treatment in sports medicine and chronic fatigue syndrome; The neuroprotective effect provides new treatment strategies for neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, etc; The role of anti-tumor and alleviating cachexia provides support for the comprehensive management of cancer patients.
At present, salidroside is still in the early stages of clinical research, facing challenges such as dose optimization, administration methods, and long-term safety evaluation. In the future, we should strengthen the in-depth analysis of its pharmacological mechanism, combine modern medicinal chemistry and pharmaceutical technology, and develop efficient and safe salidroside derivatives and compound preparations. At the same time, large-scale, multi center clinical trials will be conducted to verify its efficacy and safety, laying a solid foundation for its transformation into commonly used clinical drugs.
In addition, the potential applications of salidroside in metabolic diseases, immune regulation, and psychiatric disorders are also worth further exploration. Combining precision medicine and molecular targeted therapy concepts, salidroside is expected to become an important breakthrough in the development of natural product drugs.
As the main active ingredient in Rhodiola rosea, salidroside exhibits a wide range of biological activities and good medicinal properties due to its unique chemical structure and multi-target pharmacological effects. Its research progress in anti fatigue, neuroprotection, and alleviation of tumor cachexia provides valuable scientific basis for natural product pharmacology and new drug development.
In the future, with the continuous revelation of molecular mechanisms and the deepening of clinical research, salidroside is expected to become a new natural medicine for the treatment of various diseases. Strengthening its pharmacokinetic optimization and safety evaluation will promote its clinical application and advance the widespread use of natural products in modern medicine.
