|Source:||The rhizomes of Cistanche tubulosa (Schenk) Wight|
|Biological Activity or Inhibitors:||1. Echinacoside can provide a pronounced protection against GalN/LPS-induced acute liver injury in mice.
2. Echinacoside could improve the hematopoietic function of bone marrow in 5-FU-induced myelosuppression mice.
3. Echinacoside could increase viability of rat pheochromocytoma PC12 cells injured by Aβ and suppress the increase in intracellular reactive oxygen species (ROS) triggered by Aβ.
4. Echinacoside inhibits against 6-OHDA-induced neurotoxicity, the mechanism may be involve in attenuating mitochondrial dysfunction and inflammatory responses by reducing ROS production.
5. Transient treatment with Echinacoside inhibits cytochrome c release and caspase-3 activation caused by ensuing rotenone exposure via activating Trk-extracellular signal-regulated kinase (ERK) pathway in neuronal cells.
6. Echinacoside can trigger cells in the G1 phase to enter the S phase and G2 phase, and can improve ROS degradation, it can protect cells from DNA damage, suggest that echinacoside has potential anti-senescence activity.
7. Echinacoside for 12 weeks can effectively and safely prevent vehicle (OVX)-induced osteoporosis in rats via increasing the osteoprotegerin (OPG)/receptor activator of nuclear factor- κ B ligand (RANKL) ratio.
8. Echinacoside can inhibit hypoxia-induced proliferation of PASMCs, which is associated with of PASMCs and improvement of hypoxia, it may be a potential agent for prevention and treatment of hypoxia-induced .
9. Echinacoside induces apoptotic cancer cell death by inhibiting the nucleotide pool sanitizing enzyme MTH1.
|Solvent:||DMSO, Pyridine, Methanol, Ethanol, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever 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 -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||1.2711 mL||6.3555 mL||12.711 mL||25.422 mL||31.7775 mL|
|5 mM||0.2542 mL||1.2711 mL||2.5422 mL||5.0844 mL||6.3555 mL|
|10 mM||0.1271 mL||0.6356 mL||1.2711 mL||2.5422 mL||3.1778 mL|
|50 mM||0.0254 mL||0.1271 mL||0.2542 mL||0.5084 mL||0.6356 mL|
|100 mM||0.0127 mL||0.0636 mL||0.1271 mL||0.2542 mL||0.3178 mL|
Scand J Gastroenterol. 2014 Aug;49(8):993-1000.
|Echinacoside ameliorates D-galactosamine plus lipopolysaccharide-induced acute liver injury in mice via inhibition of apoptosis and inflammation.[Pubmed: 24797709]|
|OBJECTIVE: This study aimed to investigate the protective effects of Echinacoside, one of the phenylethanoids isolated from the stems of Cistanche salsa, a Chinese herbal medicine, on D-galactosamine (GalN) and lipopolysaccharide (LPS)-induced acute liver injury in mice. Pretreatment with Echinacoside remarkably improved the survival rate of GalN/LPS-treated mice and attenuated acute hepatotoxicity, as demonstrated by decreased ALT levels and improved histological signs. Echinacoside shows both anti-apoptotic and anti-inflammatory properties, characterized by a substantial inhibition of hepatocyte apoptosis and a significant reduction in the inflammatory markers, including myeloperoxidase, extracellular nucleosomes, high-mobility group box 1, and inflammatory cytokines in the plasma of mice, which may be important mechanisms related to its protective effect. CONCLUSION: Our results suggest that Echinacoside can provide a pronounced protection against GalN/LPS-induced acute liver injury in mice, which may complement the available strategies for management of acute liver damage in clinical settings.|
Evid Based Complement Alternat Med. 2015;2015:189239.
|Echinacoside Protects against 6-Hydroxydopamine-Induced Mitochondrial Dysfunction and Inflammatory Responses in PC12 Cells via Reducing ROS Production.[Pubmed: 25788961]|
|Echinacoside (ECH) is a phenylethanoid glycoside isolated from the stems of Cistanche salsa, showing a variety of neuroprotective effects in previous studies. The present study was to investigate its effect against 6-OHDA-induced neurotoxicity and possible mechanisms in PC12 cells. The results showed that 6-OHDA reduced cell viability, decreased oxidation-reduction activity, decreased mitochondrial membrane potential, and induced mitochondria-mediated apoptosis compared with untreated PC12 cells. However, Echinacoside treatment significantly attenuated these changes induced by 6-OHDA. In addition, Echinacoside also could significantly alleviate the inflammatory responses induced by 6-OHDA. Further research showed that Echinacoside could reduce 6-OHDA-induced ROS production in PC12 cells. These results suggest that the underlying mechanism of Echinacoside against 6-OHDA-induced neurotoxicity may be involve in attenuating mitochondrial dysfunction and inflammatory responses by reducing ROS production.|
Life Sci. 2015 Feb 15;123:86-92.
|Echinacoside improves hematopoietic function in 5-FU-induced myelosuppression mice.[Pubmed: 25623854]|
|AIMS: We aimed to investigate the effects of Echinacoside (ECH) on hematopoietic function in 5-FU-induced bone marrow depression mice. MAIN METHODS: In vitro, after stimulation with Echinacoside, the proliferation ability of bone marrow (BM) cells and bone marrow stromal cells (BMSCs) derived from myelosuppression mice were assessed by CCK8 assay and morphology, respectively. In vivo, 5-FU-induced myelosuppression or control mice were intragastrically administrated with either Echinacoside at 15 mg/kg or the equal volume of normal saline daily for 12 days before BM cells were isolated for colony-forming cell assay. Meanwhile, BMSCs were cultured for 4 weeks before cells were observed for growth pattern, cell culture supernatants were collected for GM-CSF secretion by ELISA, and RNA of the cells were extracted for EPO and GM-CSF RT-PCR. BM cells or BMSCs stimulated with Echinacoside for 24 h or 48 h were collected for protein extraction and Western blotting. KEY FINDINGS: Echinacoside stimulated the growth of BM cells but not BMSCs derived from 5-FU treated mice. The intragastric administration of Echinacoside in 5-FU treated mice could increase the number of total hematopoietic progenitor cells and GM progenitor cells to healthy control mice level, but not BFU progenitor cells. BMSCs from Echinacoside treated myelosuppression mice grew more vigorously and expressed more GM-CSF, but not EPO. Echinacoside activated the PI3K signaling pathway in 5-FU suppressed BM cells. SIGNIFICANCE: Echinacoside could improve the hematopoietic function of bone marrow in 5-FU-induced myelosuppression mice. Echinacoside can be considered as an alternative effective therapy for patients during chemotherapy or HSC transplantation.|
J Neurochem. 2013 Feb;124(4):571-80.
|Transient exposure to echinacoside is sufficient to activate Trk signaling and protect neuronal cells from rotenone.[Pubmed: 23189969]|
|We reported that Echinacoside, a small natural compound, elicits neuroprotection by activating Trk receptors and their downstream signal pathways. Echinacoside is the major active component of Cistanches Herba, a widely used Chinese herb with neuroprotective effects. We showed in this study that transient exposure to Echinacoside is sufficient to protect neuronal cells and non-neuronal cells over-expressed with TrkA or TrkB against rotenone injury. Additional investigations on the mechanisms underlying suggested that transient treatment with Echinacoside inhibits cytochrome c release and caspase-3 activation caused by ensuing rotenone exposure via activating Trk-extracellular signal-regulated kinase (ERK) pathway in neuronal cells. As Echinacoside is able to cross the blood-brain barrier freely, it may have a promising potential in neurodegenerative diseases treatment.|
Int J Biol Macromol. 2015 Jan;72:243-53.
|Echinacoside inhibits amyloid fibrillization of HEWL and protects against Aβ-induced neurotoxicity.[Pubmed: 25193102]|
|We investigated the protection provided by Echinacoside against neurotoxicity induced by β-amyloid protein (Aβ). Through spectroscopic analyses, electron microscopy, cell viability assay, and hemolysis assay, we found that Echinacoside dose dependently inhibited HEWL aggregation, and this inhibition occurred in different fiber-forming stages. Echinacoside could also scavenge the DPPH and OH free radicals in a concentration-dependent manner. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and 2',7'-dichlorodihydrofluoresceindiacetate (DCFH-DA) fluorescent measurement results indicated that Echinacoside could increase viability of rat pheochromocytoma PC12 cells injured by Aβ and suppress the increase in intracellular reactive oxygen species (ROS) triggered by Aβ. The present study findings facilitate a better understanding of the interaction between Echinacoside and amyloid-forming proteins and also shed light on the protection of Echinacoside against amyloid fibril-induced neuronal cell death.|
Evid Based Complement Alternat Med. 2013;2013:926928.
|Efficacy and safety of echinacoside in a rat osteopenia model.[Pubmed: 23573159 ]|
|This study aimed to investigate the efficacy and safety of Echinacoside (ECH) using an osteopenia rat model. Forty-eight 6-month-old female Sprague-Dawley rats were randomly divided into one sham-operated group (SHAM) and five OVX (ovariectomized) subgroups: SHAM with vehicle 0.5% carboxymethylcellulose sodium (0.5% CMC-Na) and OVX with vehicle (OVX), OVX with 17 β -estradiol (E2), and OVX with ECH of graded doses (ECH-L, ECH-M, and ECH-H). The effects of ECH and E2 on serum biochemical parameters, bone mineral density (BMD), bone biomechanical properties, bone microarchitecture, and immunohistochemistry were examined, and safety assessments were also evaluated. The results showed that ECH treatments improved total femur BMD, bone microarchitecture, and biomechanical properties and decreased serum marker levels in comparison to OVX group. Moreover, ECH administration significantly increased osteoprotegerin (OPG) level, and decreased receptor activator of nuclear factor- κ B ligand (RANKL) level in serum, as well as in proximal femur. Importantly, ECH treatment ameliorated the lipid parameters without the overall incidences of adverse events of uterus and mammary gland compared to OVX and SHAM groups. This study demonstrated that administration of ECH for 12 weeks can effectively and safely prevent OVX-induced osteoporosis in rats via increasing the OPG/RANKL ratio.|
Pharmazie. 2009 Nov;64(11):752-4.
|Echinacoside retards cellular senescence of human fibroblastic cells MRC-5.[Pubmed: 20099521]|
|In this study, effects of Echinacoside, one of the phenylethanoids isolated from the stems of Cistanches salsa, a Chinese traditional herbal medicine, on human embryo lung fibroblastic MRC-5 cells, was investigated. Activity of cell proliferation was evaluated with Alamar Blue, showing that treatment with Echinacoside could retard the senescence. Flow cytometry results show that Echinacoside could trigger cells in the G1 phase to enter the S phase and G2 phase, and could improve ROS degradation. The results from comet assay indicate that Echinacoside could protect cells from DNA damage, partly elucidating the mechanism of its effects. All of the above results suggest that Echinacoside has potential anti-senescence activity.|
J Pharmacol Sci. 2014;126(2):155-63.
|Antiproliferative effect of echinacoside on rat pulmonary artery smooth muscle cells under hypoxia.[Pubmed: 25341567]|
|The main purpose of this study is to evaluate the effect of Echinacoside (ECH) on hypoxia-induced proliferation of rat pulmonary artery smooth muscle cells (PASMCs) and the underlying mechanism. PASMCs were incubated under normoxia (nor), hypoxia (hyp), hypoxia + 0.35 mM ECH (hyp + ECH0.35), or hypoxia + 0.4 mM ECH (hyp + ECH0.4) for 24 h. Cell viability was assessed by MTS assays. The morphology of apoptosis was observed by DAPI staining, and apoptosis was quantified by flow cytometric analysis. Caspase-3 activity was determined by immunohistochemistry and real-time PCR, and the expressions of HIF-1α, Bax, Bcl-2, and Fas were determined by real-time PCR. Hypoxia induced significant proliferation of PASMCs, which could be inhibited by ECH in a concentration-dependent manner. This was associated with apoptosis of PASMCs. Z-DEVD-FMK could partly reduce the suppression effect of ECH; protein and gene expression of caspase-3 were significantly higher in the hyp + ECH0.4 and hyp + ECH0.35 groups. ECH significantly increased the expressions of Bax and Fas, but decreased the expressions of Bcl-2 and HIF-1α. ECH could inhibit hypoxia-induced proliferation of rat PASMCs, which is associated with apoptosis of PASMCs and improvement of hypoxia. ECH might be a potential agent for prevention and treatment of hypoxia-induced PAH.|
Onco Targets Ther. 2015 Dec 8;8:3649-64.
|Echinacoside induces apoptotic cancer cell death by inhibiting the nucleotide pool sanitizing enzyme MTH1.[Pubmed: 26677335 ]|
|Echinacoside, a compound derived from the medicinal plants Cistanche and Echinacea, effectively inhibited the catalytic activity of MTH1 in an in vitro assay. Treatment of various human cancer cell lines with Echinacoside resulted in a significant increase in the cellular level of oxidized guanine (8-oxoguanine), while cellular reactive oxygen species level remained unchanged, indicating that Echinacoside also inhibited the activity of cellular MTH1. Consequently, Echinacoside treatment induced an immediate and dramatic increase in DNA damage markers and upregulation of the G1/S-CDK inhibitor p21, which were followed by marked apoptotic cell death and cell cycle arrest in cancer but not in noncancer cells. Taken together, these studies identified a natural compound as an MTH1 inhibitor and suggest that natural products can be an important source of anticancer agents.|