|Description:||1. Acteoside is a lipase inhibitor, has anti-obesity properties.|
2. Acteoside has neuroprotective activity, can promote nerve growth factor and tropomycin receptor kinase A expression.
3. Acteoside has anti-inflammatory activity, it significantly inhibits arachidonic acid release and prostaglandin E2 production induced by 0.5 microM melittin.
4. Acteoside has antioxidant activity, can protect the cells from X‑ray induced damage through enhancing the scavenging activity of ROS, decreasing the Bax/Bcl-2 ratio and downregulating the activity of procaspase-3, as well as modulating the mitogen‑activated protein kinase signaling pathways.
5. Acteoside exhibits anticancer, cytotoxic and antimetastatic activities, it is an antiestrogen in breast cancer cells and osteoblasts.
6. Acteoside has protective effects against the carbon tetrachloride-induced hepatotoxicity, the mechanisms possibly related to its ability to block the P450-mediated carbon tetrachloride bioactivation and free radical scavenging effects.
7. Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation via inducing cell cycle arrest at G0/G1 phase and differentiation into monocyte.
8. Acteoside and its analogs have antioxidant and antihypertensive activities, it is a new antihypertensive drug.
9. Acteoside has analgesic activity, it as the Analgesic Principle of Cedron (Lippia hriphylla), a Peruvian Medicinal Plant.
|Targets:||IL Receptor | Bcl-2/Bax | Caspase | p53 | TNF-α | Mdm2 | Estrogen receptor | NO | NOS | ROS | ERK | JNK | P450 (e.g. CYP17) | Calcium Channel | PGE | CDK | p21 | Progestogen receptor|
|Source:||The herbs of Cistanche deserticola Y.C. Ma|
|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.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|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||1.601 mL||8.0051 mL||16.0102 mL||32.0205 mL||40.0256 mL|
|5 mM||0.3202 mL||1.601 mL||3.202 mL||6.4041 mL||8.0051 mL|
|10 mM||0.1601 mL||0.8005 mL||1.601 mL||3.202 mL||4.0026 mL|
|50 mM||0.032 mL||0.1601 mL||0.3202 mL||0.6404 mL||0.8005 mL|
|100 mM||0.016 mL||0.0801 mL||0.1601 mL||0.3202 mL||0.4003 mL|
Int Immunopharmacol. 2015 May;26(1):23-9.
|Acteoside attenuates TSLP-induced mast cell proliferation via down-regulating MDM2.[Pubmed: 25773666]|
|Acteoside (verbascoside) is extensively distributed in Abeliophyllum distichum and has antimicrobial and anti-inflammatory properties. Thymic stromal lymphopoietin (TSLP) has a pivotal function in the pathogeneses of inflammatory diseases through increasing the mast cell proliferation via the activation of murine double minute 2 (MDM2). Here, we investigate whether Acteoside attenuates the MDM2 expression in a TSLP-stimulated human mast cell line (HMC-1 cells). In these cells, TSLP induced the up-regulation of MDM2 and the down-regulation of p53; however, in the TSLP-stimulated HMC-1 cells, the Acteoside down-regulated the MDM2 and up-regulated the p53. Increases in the phosphorylation of the single transducer and activation of transcription 6 and 5 via TSLP are decreased by Acteoside. The interleukin (IL)-13 (a mast cell growth factor), IL-6, tumor necrosis factor-α, and IL-1β levels are significantly reduced by the Acteoside in the TSLP-stimulated HMC-1 cells, and the Acteoside significantly induces the activation of caspase-3, the cleavage of poly-ADP-ribose polymerase, and the reduction of the procaspase-3 and Bcl2. Furthermore, the mRNA expressions of the TSLP receptor and IL-7 receptor that increase due to TSLP are reduced by the Acteoside. In conclusion, these results indicate that Acteoside is a specific regulator of MDM2 activation in TSLP-stimulated mast cells, which indicates its potential use for the treatment of mast cell-mediated inflammatory diseases.|
J Steroid Biochem Mol Biol. 2006 Jan;98(1):63-71.
|Acteoside and martynoside exhibit estrogenic/antiestrogenic properties.[Pubmed: 16198557 ]|
|Acteoside and martynoside are plant phenylpropanoid glycosides exhibiting anticancer, cytotoxic and antimetastatic activities. We investigated their potential to activate estrogen receptor isoforms ERalpha and ERbeta in HeLa cells transfected with an estrogen response element (ERE)-driven luciferase (Luc) reporter gene and an ERalpha or ERbeta expression vector. Their estrogenic/antiestrogenic effects were also assessed in breast cancer cells (MCF7), endometrial cancer cells (Ishikawa) and osteoblasts (KS483), by measuring IGFBP3 levels, cell viability and number of mineralized nodules, respectively, seeking for a natural selective estrogen receptor modulator (SERM). Acteoside and martynoside antagonized both ERalpha and ERbeta (p<0.001), whereas they reversed the effect of E(2) mainly via ERalpha (p<0.001). Martynoside was a potent antiestrogen in MCF-7 cells, increasing, like ICI182780, IGFBP3 levels via the ER-pathway. In osteoblasts, martynoside induced nodule mineralization, which was abolished by ICI182780, implicating an ER-mediated mechanism. Furthermore, its antiproliferative effect on endometrial cells suggests that martynoside may be an important natural SERM. Acteoside was an antiestrogen in breast cancer cells and osteoblasts, without any effect on endometrial cells. Our study suggests that the nature is rich in selective ERalpha and ERbeta ligands, the discovery of which may lead to the development of novel neutraceutical agents.|
Phytother Res. 2015 Apr 21.
|The Mechanism of Memory Enhancement of Acteoside (Verbascoside) in the Senescent Mouse Model Induced by a Combination of d-gal and AlCl3.[Pubmed: 25900087]|
|Acteoside (verbsacoside), one of the main active phenylethanoid glycosides from Cistanche deserticola, is known to have antioxidant and neuroprotective activity, and herbs containing it are used to enhance memory. However, there is relatively little direct experimental evidence to support the use of Acteoside in Alzheimer's disease (AD). The purpose of this study was to elucidate the effects of Acteoside in improving learning and memory, using a mouse model of senescence induced by a combination of d-galactose and AlCl3 , and investigate its potential mechanisms compared with the positive controls vitamin E and piracetam. Acteoside was administered intragastrically at doses of 30, 60 and 120 mg/kg/day for 30 days after AD was induced. Memory function was evaluated using a step-down test. The number of neuron was analysed by haematoxylin and eosin staining and the number of Nissl bodies by Nissl staining. The expression of caspase-3 protein in hippocampus was detected by immunohistochemistry and western blot. Nitric oxide and total nitric oxide synthase level in hippocampus were also assessed. Our results showed that the latency of step down was shortened in AD model mice and the number of errors decreased after treatment with all doses of Acteoside. Neurons and Nissl bodies in the hippocampus were increased significantly with higher doses (60 and 120 mg/kg/day) of Acteoside. The content of nitric oxide, the activity of nitric oxide synthase and the expression of caspase-3 protein were decreased by 120 mg/kg/day Acteoside compared with that of the AD model group. Our results support the results obtained previously using the Morris maze test in the same mouse model of senescence, and the use of traditional medicinal herbs containing Acteoside for neuroprotection and memory loss.|
Mol Med Rep. 2015 Apr 16.
|Protective effects of acteoside against X‑ray‑induced damage in human skin fibroblasts.[Pubmed: 25892089]|
|To investigate the protective effects of Acteoside against apoptosis induced by X‑ray radiation in human skin fibroblasts (HSFs), the cells were divided into the following groups: Control group; X‑ray radiation group; Acteoside group, in which the confluent cells were preincubated with 50 µg/ml Acteoside for 2 h followed by radiation; and positive control group, in which the cells were preincubated with 50 µg/ml paeoniflorin followed by radiation. For the radiation, HSF cells preincubated with Acteoside or paeoniflorin were exposed to X‑ray beams at a dose‑rate of 3 Gy/min (16 Gy in total). Cell viability, apoptosis and intracellular alteration of redox were monitored by MTT and ﬂow cytometry. Compared with the radiation group, the number of cells arrested at the G0/G1 phase was significantly reduced in the Acteoside and paeoniflorin groups, respectively (P<0.05). X‑ray radiation induced marked apoptosis in HSF cells and Acteoside reversed this effect. Compared with the radiation group, the generation of intracellular reactive oxygen species (ROS) was abrogated by pre‑incubation with Acteoside or paeoniflorin (P<0.05). In addition, the upregulation of pro‑caspase‑3 induced by radiation was reversed by Acteoside or paeoniflorin. Radiation could induce upregulation of Bax and downregulation of Bcl‑2; however, it was reversed completely after administration of Acteoside or paeoniflorin. Furthermore, the enhanced expression of ERK and JNK induced by radiation was reversed by Acteoside or paeoniflorin. Acteoside could protect the cells from X‑ray induced damage through enhancing the scavenging activity of ROS, decreasing the Bax/Bcl‑2 ratio and downregulating the activity of procaspase‑3, as well as modulating the mitogen‑activated protein kinase signaling pathways.|
Food Chem. 2014 Jan 1;142:306-10.
|Acteoside: a lipase inhibitor from the Chinese tea Ligustrum purpurascens kudingcha.[Pubmed: 24001846 ]|
|Acteoside is the most abundant and major active component of Ligustrum purpurascens (kudingcha tea). Here, we explored the anti-obesity properties of Acteoside by investigating its effect on lipase activity. Characterization of Acteoside and lipase by fluorescence spectroscopy, isothermal titration calorimetry and circular dichroism revealed that Acteoside might act as a non-competitive lipase inhibitor. Acteoside bound to lipase at Ka=1.88×10(4)lmol(-1). Thermodynamic features suggested that the binding interaction was mainly hydrophobic and the complex was stabilized by hydrogen bonding, with 1:1 interaction of Acteoside and lipase. Furthermore, docking results supported experimental findings and revealed hydrogen bonding with Lys271, Leu272 and Thr68 of lipase. This non-covalent bonding between Acteoside and lipase alters the molecular conformation of lipase, which decreases the enzyme catalytic activity.|
Life Sci. 2004 Jan 9;74(8):1051-64.
|Protective effect of acteoside on carbon tetrachloride-induced hepatotoxicity.[Pubmed: 14672760]|
|This study investigated the protective effects of Acteoside, a phenylethanoid glycoside, on the carbon tetrachloride-induced hepatotoxicity as well as the possible mechanisms involved in this protection in mice. Pretreatment with Acteoside prior to the administration of carbon tetrachloride significantly prevented the increased serum enzymatic activities of alanine and aspartate aminotransferase in a dose-dependent manner. In addition, pretreatment with Acteoside significantly prevented the increase in hepatic malondialdehyde formation and the depletion of the reduced glutathione content in the liver of carbon tetrachloride-intoxicated mice. Carbon tetrachloride-induced hepatotoxicity was also essentially prevented, as indicated by a liver histopathologic study. The effects of Acteoside on cytochrome P450 (P450) 2E1, the major isozyme involved in carbon tetrachloride bioactivation were also investigated. Treatment of the mice with Acteoside resulted in a significant decrease in the P450 2E1-dependent pnitrophenol and aniline hydroxylation in a dose-dependent manner. Consistent with these observations, the P450 2El protein levels were also lower. Acteoside exhibited anti-oxidant effects on FeCl2-ascorbate induced lipid peroxidation in a mouse liver homogenate, and on superoxide radical scavenging activity. These results suggest that the protective effects of Acteoside against the carbon tetrachloride-induced hepatotoxicity possibly involve mechanisms related to its ability to block the P450-mediated carbon tetrachloride bioactivation and free radical scavenging effects.|
Arch Pharm Res. 2006 Jun;29(6):508-13.
|The effect of acteoside on histamine release and arachidonic acid release in RBL-2H3 mast cells.[Pubmed: 16833020]|
|The effect of Acteoside, a phenylpropanoid glycoside isolated from Clerodendron trichotomum Thunberg, on histamine and arachidonic acid release was investigated in RBL 2H3 cells. Histamine was dose-dependently released from RBL 2H3 cells by melittin, arachidonic acid and thapsigargin. In extracellular Ca2+-free solution, basal secretion of histamine increased by two fold. The response of histamine release to melittin and thapsigargin in Ca2+-free solution was significantly decreased, whereas the response to arachidonic acid was significantly increased as compared with those in normal solution. Acteoside inhibited histamine release induced by melittin, arachidonic acid and thapsigargin in a dose-dependent manner in the presence or absence of extracellular Ca2+. However, the inhibitory activity of Acteoside was more potent in normal solution than that in Ca2+-free solution. These data suggest that inhibitory mechanism of Acteoside on histamine release may be related to extracellular Ca2+. On the other hand, Acteoside significantly inhibited arachidonic acid release and prostaglandin E2 production induced by 0.5 microM melittin. It is possible that Acteoside may be developed as an anti-inflammatory agent.|
Bot. Stud., 2012, 53(4):421-9.
|Antioxidant and antihypertensive activities of acteoside and its analogs.[Reference: WebLink]|
|Acteoside (Act), a phenylethanoid glycoside, is an active compound in several plants and traditional herbal medicines. Act along with its structural isomer, isoActeoside (Isoact), and an analog, 6-O-acetylActeoside (6-O-acetylact), were used in the study to investigate the antioxidant, anti-angiotensin-converting enzyme (ACE), and hemolysis inhibitory activities in vitro and antihypertensive activity against spontaneously hypertensive rats (SHR) in vivo. We showed that Act, Isoact, and 6-O-acetylact effectively scavenged 1,1-diphenyl- 2-picryl-hydrazyl radicals (with IC50 at 11.4, 9.48, and 9.55 μM, respectively) and superoxide radicals (with IC50 at 66.0, 38.5, and 39.1 μM, respectively). As Isoact and 6-O-acetylact had similar radical-scavenging activities, only Act and Isoact were used for following studies. Both Act and Isoact inhibited xanthine oxidase activity with IC50 at 53.3 and 62.2 μM, respectively. Both Act and Isoact also significantly inhibited ACE activity and the hemolysis induced by 2,2'-azo-bis(2-amidinopropane)dihydrochloride, but the effects of Act were stronger than Isoact. We then orally administered a single dose of Act or Isoact (10 mg/Kg body weight) to SHR and measured the changes of systolic blood pressure (SBP) and diastolic blood pressure (DBP) over 24 h. Act, but not Isoact, showed antihypertensive activity in lowering SBP and DBP. The results suggest the potential usefulness of Act as a health food product for antioxidant protection and blood pressure regulation.|
Chem. Pharm. Bull., 1997, 45(3):499-504.
|Acteoside as the Analgesic Principle of Cedron (Lippia hriphylla), a Peruvian Medicinal Plant.[Reference: WebLink]|
|Acteoside (verbascoside) was isolated as an analgesic principle from Cedron (leaves and stem of Lippia triphylla (L'HER) O. KUNTZE; Verbenaceae), a Peruvian medicinal plant, by activity-guided separation. The compound exhibited analgesia on acetic acid-induced writhing and on tail pressure pain in mice by the oral administration of 300mg/kg and 100mg/kg, respectively. Acteoside also caused weak sedation by its effect on the prolongation of pentobarbital-induced anesthesia and on the depression of locomotion enhanced by methamphetamine. An intravenous injection of Acteoside reduced the effective dose to 2mg/kg by the writhing method. Thirteen related compounds were tested for the activity by intravenous and oral administration to obtain information on the active structure.|
Carcinogenesis. 2007 Sep;28(9):1928-36.
|Acteoside inhibits human promyelocytic HL-60 leukemia cell proliferation via inducing cell cycle arrest at G0/G1 phase and differentiation into monocyte.[Pubmed: 17634406 ]|
|We investigated the in vitro effects of Acteoside on the proliferation, cell cycle regulation and differentiation of HL-60 human promyelocytic leukemia cells. Acteoside inhibited the proliferation of HL-60 cells in a concentration- and time-dependent manner with an IC50, approximately 30 microM. DNA flow cytometric analysis indicated that Acteoside blocked cell cycle progression at the G1 phase in HL-60 human promyelocytic leukemia cells. Among the G1 phase cell cycle-related proteins, the levels of cyclin-dependent protein kinase (CDK)2, CDK6, cyclin D1, cyclin D2, cyclin D3 and cyclin E were reduced by Acteoside, whereas the steady-state level of CDK4 was unaffected. The protein and mRNA levels of CDK inhibitors (cyclin-dependent kinase inhibitors), such as p21(CIP1/WAF1) and p27(KIP1), were gradually increased after Acteoside treatment in a time-dependent manner. In addition, Acteoside markedly enhanced the binding of p21(CIP1/WAF1) and p27(KIP1) to CDK4 and CDK6, resulting in the reduction of CDK2, CDK4 and CDK6 activities. Moreover, the hypophosphorylated form of retinoblastoma increased, leading to the enhanced binding of protein retinoblastoma (pRb) and E2F1. Our results further suggest that Acteoside is a potent inducer of differentiation of HL-60 cells based on biochemical activities and the expression level of CD14 cell surface antigen. In conclusion, the onset of Acteoside-induced G1 arrest of HL-60 cells prior to the differentiation appears to be tightly linked to up-regulation of the p21(CIP1/WAF1) and p27(KIP1) levels and decreases in the CDK2, CDK4 and CDK6 activities. These findings, for the first time, reveal the mechanism underlying the anti-proliferative effect of Acteoside on human promyelocytic HL-60 cells.|