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Salidroside

$43

  • Brand : BIOFRON

  • Catalogue Number : BF-S3012

  • Specification : 98%

  • CAS number : 10338-51-9

  • Formula : C14H20O7

  • Molecular Weight : 300.3

  • PUBCHEM ID : 159278

  • Volume : 25mg

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Catalogue Number

BF-S3012

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

300.3

Appearance

White crystalline powder

Botanical Source

Ligustrum lucidum,Rehmannia glutinosa,Lamiophlomis rotata,Rhodiola crenulata,Akebia quinata

Structure Type

Phenolics

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC(=CC=C1CCOC2C(C(C(C(O2)CO)O)O)O)O

Synonyms

SALIDROSIDE RHODIOLOSIDE/2-(4-Hydroxyphenyl)ethyl α-D-glucopyranoside/RHODIOLOSIDE/Salisorosides Rosavin/Salidroside/RhodiolaCrenulataExtract/rhodosin/TWEEN 20 EXTRA PURE/β-D-Glucopyranoside, 2-(4-hydroxyphenyl)ethyl/2-(4-Hydroxyphenyl)ethyl β-D-glucopyranoside/α-D-Glucopyranoside, 2-(4-hydroxyphenyl)ethyl/RHODIOLAEXTRACT

IUPAC Name

(2R,3S,4S,5R,6R)-2-(hydroxymethyl)-6-[2-(4-hydroxyphenyl)ethoxy]oxane-3,4,5-triol

Density

1.5±0.1 g/cm3

Solubility

Methanol; Ethanol; Water

Flash Point

286.2±30.1 °C

Boiling Point

549.5±50.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:10338-51-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

28478514

Abstract

Salidroside is being investigated for its therapeutic potential in stroke because it is neuroprotective over an extended therapeutic window of time. In the present study, we investigated the mechanisms underlying the anti-inflammatory effects of salidroside (50 mg/kg intraperitoneally) in rats, given 1 h after reperfusion of a middle cerebral artery that had been occluded for 2 h. After 24 h, we found that salidroside increased the neuronal nuclear protein NeuN and reduced the marker of microglia and macrophages CD11b in the peri-infarct area of the brain. Salidroside also decreased IL-6, IL-1β, TNF-α, CD14, CD44, and iNOs mRNAs. At the same time, salidroside increased the ratio of phosphorylated protein kinase B (p-Akt) to total Akt. The phosphoinositide 3-kinase (PI3K) inhibitor LY294002 prevented this increase in p-Akt and reversed the inhibitory effects of salidroside on CD11b and inflammatory mediators. Salidroside also elevated the protein levels of hypoxia-inducible factor (HIF) subunits HIF1α, HIF2α, HIF3α, and of erythropoietin (EPO). The stimulatory effects of salidroside on HIFα subunits were blocked by LY294002. Moreover, YC-1, a HIF inhibitor, abolished salidroside-mediated increase of HIF1α and prevented the inhibitory effects of salidroside on CD11b and inflammatory mediators. Taken together, our results provide evidence for the first time that all three HIFα subunits and EPO can be regulated by PI3K/Akt in cerebral tissue, and that salidroside entrains this signaling pathway to induce production of HIFα subunits and EPO, one or more of which mediate the anti-inflammatory effects of salidroside after cerebral IRI.

KEYWORDS

cerebral ischemia; hypoxia-inducible factors; inflammation; phosphoinositide 3-kinase; salidroside.

Title

Salidroside Inhibits Inflammation Through PI3K/Akt/HIF Signaling After Focal Cerebral Ischemia in Rats

Author

Yicong Wei 1 , Haimian Hong 1 , Xiaoqin Zhang 1 , Wenfang Lai 1 , Yingzheng Wang 1 , Kedan Chu 1 , John Brown 1 , Guizhu Hong 1 , Lidian Chen 2

Publish date

2017 Aug

PMID

29148269

Abstract

Spinal cord injury (SCI) is a severe neurological disease; however, few drugs have been proved to treat SCI effectively. Neuroinflammation is the major pathogenesis of SCI secondary injury and considered to be the therapeutic target of SCI. Salidroside (Sal) has been reported to exert anti-inflammatory effects in airway, adipose and myocardial tissue; however, the role of Sal in SCI therapeutics has not been clarified. In this study, we showed that Sal could improve the functional recovery of spinal cord in rats as revealed by increased BBB locomotor rating scale, angle of incline, and decreased cavity of spinal cord injury and apoptosis of neurons in vivo. Immunofluorescence double staining of microglia marker and M1/M2 marker demonstrated that Sal could suppress M1 microglia polarization and activate M2 microglia polarization in vivo. To verify how Sal exerts its effects on microglia polarization and neuron protection, we performed the mechanism study in vitro in microglia cell line BV-2 and neuron cell line PC12. The results showed that Sal prevents apoptosis of PC12 cells in coculture with LPS-induced M1 BV-2 microglia, also the inflammatory secretion phenotype of M1 BV-2 microglia was suppressed by Sal, and further studies demonstrated that autophagic flux regulation through AMPK/mTOR pathway was involved in Sal regulated microglia polarization after SCI. Overall, our study illustrated that Sal could promote spinal cord injury functional recovery in rats, and the mechanism may relate to its microglia polarization modulation through AMPK-/mTOR-mediated autophagic flux stimulation.

KEYWORDS

AMPK; M1 polarization; M2 polarization; autophagic flux; microglia; salidroside; spinal cord injury.

Title

Salidroside Attenuates Neuroinflammation and Improves Functional Recovery After Spinal Cord Injury Through Microglia Polarization Regulation

Author

Chenggui Wang 1 2 , Qingqing Wang 1 2 , Yiting Lou 1 2 , Jianxiang Xu 1 2 , Zhenhua Feng 1 2 , Yu Chen 1 2 , Qian Tang 1 2 , Gang Zheng 1 2 , Zengjie Zhang 1 2 , Yaosen Wu 1 2 , Naifeng Tian 1 2 , Yifei Zhou 1 2 , Huazi Xu 1 2 , Xiaolei Zhang 1 2 3

Publish date

2018 Feb

PMID

30140371

Abstract

Our previous studies suggested that salidroside could alleviate hepatic steatosis in type 2 diabetic C57BLKS/Leprdb (db/db) mice. The aim of the present study was to evaluate the therapeutic effect of salidroside on high-fat diet- (HFD-) induced nonalcoholic fatty liver disease (NAFLD) by investigating underlying mechanisms. Mice were fed with HFD or regular diet, randomly divided into two groups, and treated with salidroside or vehicle for 8 weeks. Then, biochemical analyses and histopathological examinations were conducted in vivo and in vitro. Salidroside administration attenuated HFD-induced obesity, blood glucose variability, and hepatic lipid deposition, markedly increasing insulin sensitivity in HFD mice. In addition, salidroside suppressed oxidative stress, thioredoxin-interacting protein (TXNIP) expression, and NLRP3 inflammasome activation in the liver. In cultured hepatocytes, salidroside dose dependently regulated lipid accumulation, reactive oxygen species (ROS) generation, and NLRP3 inflammasome activation as well as improved AMP-activated protein kinase (AMPK) activity and insulin sensitivity. The inhibition of AMPK activation by inhibitor or short interfering RNA (siRNA) resulted in the suppression of the beneficial effects of salidroside in hepatocytes. Our findings demonstrated that salidroside protects against NAFLD by improving hepatic lipid metabolism and NLRP3 inflammasome activation, and these actions are related to the regulation of the oxidative stress and AMPK-dependent TXNIP/NLRP3 pathways.

Title

Salidroside Attenuates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease via AMPK-Dependent TXNIP/NLRP3 Pathway

Author

Tao Zheng 1 2 3 4 , Xiaoyan Yang 3 , Wenjin Li 1 3 , Qibin Wang 2 4 , Li Chen 2 4 , Dan Wu 1 3 , Fang Bian 1 3 , Shasha Xing 1 3 , Si Jin 1 3 5

Publish date

2018 Jul 22


Description :

Salidroside is a prolyl endopeptidase Inhibitor. Salidroside alleviates cachexia symptoms in mouse models of cancer cachexia via activating mTOR signalling.