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J Chromatogr B Analyt Tec. Bio. Life Sci. 2018 Feb 17;Viruses. 2017 Oct 3;9(10). Arch Biochem Biophys. 2018 Jan 15;Molecules. 2017 Jun 2;Mol Immunol. 2016 Oct;78:121-132.
Chem Biol Interact. 2016 Oct 25Biochem Pharmacol. 2017 Apr 15;Molecules 2016, 21(6), 780; 2016 Jun 17;21(6).Journal of Analytical ChemistryAug. 2017;Sci Rep. 2017 Jan 9;
J Agric Food Chem.2018 Jan 10;Br J Pharmacol.2018 Mar;J Pharm Biomed Anal. 2016 Jun 25;129:50-59. Experimental Parasitology2015 March 24.
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||Hirsutine has anticancer, cardioprotective, anti‑hypertensive and anti-arrhythmic activities, it also has vasodilatation activity, the mechanism is related to blockade of Ca2+ influx through L-type Ca2+ channels and inhibition of intracellular Ca2+ release may have no relationship with K+ channels. Hirsutine reduces the production of various neurotoxic factors in activated microglial cells and possesses neuroprotective activity in a model of inflammation-induced neurotoxicity.
||p53 | NF-kB | Akt | p38MAPK | MMP(e.g.TIMP) | Calcium Channel | Potassium Channel | NO | PGE | IL Receptor|
|Oncol Rep. 2015 Apr;33(4):2072-6. |
|Selective anticancer activity of hirsutine against HER2‑positive breast cancer cells by inducing DNA damage.[Pubmed: 25672479]|
|Hirsutine is one of the major alkaloids isolated from plants of the Uncaria genus and is known for its cardioprotective, anti‑hypertensive and anti-arrhythmic activities.
We recently reported that Hirsutine is an anti-metastatic phytochemical by targeting NF-κB activation in a murine breast cancer model.
METHODS AND RESULTS:
In the present study, we further examined the clinical utility of Hirsutine against human breast cancer. Among six distinct human breast cancer cell lines, Hirsutine showed strong cytotoxicity against HER2-positive/p53-mutated MDA-MB‑453 and BT474 cell lines. Conversely, HER2-negative/p53 wild‑type MCF-7 and ZR-75-1 cell lines showed resistance against Hirsutine-induced cytotoxicity. Hirsutine induced apoptotic cell death in the MDA-MB-453 cells, but not in the MCF-7 cells, through activation of caspases. Furthermore, Hirsutine induced the DNA damage response in the MDA-MB-453 cells, but not in the MCF-7 cells, as highlighted by the upregulation of γH2AX expression. Along with the induction of the DNA damage response, the suppression of HER2, NF-κB and Akt pathways and the activation of the p38 MAPK pathway in the MDA-MB-453 cells were observed.
Considering that there was no difference between MDA-MB-453 and MCF-7 cells in regards to irinotecan‑induced DNA damage response, our present results indicate the selective anticancer activity of Hirsutine in HER2-positive breast cancer by inducing a DNA damage response.
|Life Sci. 1992;50(7):491-8. |
|Effects of hirsutine, an antihypertensive indole alkaloid from Uncaria rhynchophylla, on intracellular calcium in rat thoracic aorta.[Pubmed: 1311793]|
|The effects of Hirsutine, an indole alkaloid from Uncaria rhynchophylla (MIQ.) Jackson, on cytosolic Ca2+ level ([Ca2+]cyt) were studied by using fura-2-Ca2+ fluorescence in smooth muscle of the isolated rat aorta.
METHODS AND RESULTS:
Noradrenaline and high K+ solution produced a sustained increase in [Ca2+]cyt. Application of Hirsutine after the increases in [Ca2+]cyt induced by noradrenaline and high K+ notably decreased [Ca2+]cyt, suggesting that Hirsutine inhibits Ca2+ influx mainly through a voltage-dependent Ca2+ channel. Furthermore, the effect of Hirsutine on intracellular Ca2+ store was studied by using contractile responses to caffeine under the Ca(2+)-free nutrient condition in the rat aorta. When Hirsutine was added at 30 microM before caffeine treatment, the agent slightly but significantly reduced the caffeine-induced contraction. When added during Ca2+ loading, Hirsutine definitely augmented the contractile response to caffeine. These results suggest that Hirsutine inhibits Ca2+ release from the Ca2+ store and increases Ca2+ uptake into the Ca2+ store, leading to a reduction of intracellular Ca2+ level.
It is concluded that Hirsutine reduces intracellular Ca2+ level through its effect on the Ca2+ store as well as through its effect on the voltage-dependent Ca2+ channel.
|Mol Med Rep. 2013 Jan;7(1):154-8. |
|Hirsutine, an indole alkaloid of Uncaria rhynchophylla, inhibits inflammation-mediated neurotoxicity and microglial activation.[Pubmed: 23117160]|
|Chronic microglial activation endangers neuronal survival through the release of various pro-inflammatory and neurotoxic factors. As such, negative regulators of microglial activation have been considered as potential therapeutic candidates to reduce the risk of neurodegeneration associated with inflammation. Uncaria rhynchophylla (U. rhynchophylla) is a traditional oriental herb that has been used for treatment of disorders of the cardiovascular and central nervous systems. Hirsutine (HS), one of the major indole alkaloids of U. rhynchophylla, has demonstrated neuroprotective potential.
METHODS AND RESULTS:
The aim of the present study was to examine the efficacy of HS in the repression of inflammation-induced neurotoxicity and microglial cell activation. In organotypic hippocampal slice cultures, HS blocked lipopolysaccharide (LPS)-related hippocampal cell death and production of nitric oxide (NO), prostaglandin (PG) E2 and interleukin-1β. HS was demonstrated to effectively inhibit LPS-induced NO release from cultured rat brain microglia. The compound reduced the LPS-stimulated production of PGE2 and intracellular reactive oxygen species. HS significantly decreased LPS-induced phosphorylation of the mitogen-activated protein kinases and Akt signaling proteins.
In conclusion, HS reduces the production of various neurotoxic factors in activated microglial cells and possesses neuroprotective activity in a model of inflammation-induced neurotoxicity.
||The herbs of Uncaria rhynchophylla
||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
||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: firstname.lastname@example.org
||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.
Recent ChemFaces New Products and Compounds
Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.PMID: 29328914
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.PMID: 29149595
Scientific Reports 2017 Dec 11;7(1):17332.doi: 10.1038/s41598-017-17427-6.PMID: 29230013
Molecules. 2017 Oct 27;22(11). pii: E1829.doi: 10.3390/molecules22111829.PMID: 29077044
J Cell Biochem. 2018 Feb;119(2):2231-2239.doi: 10.1002/jcb.26385. PMID: 28857247
Phytomedicine. 2018 Feb 1;40:37-47. doi:10.1016/j.phymed.2017.12.030PMID: 29496173
Calculate Dilution Ratios(Only for Reference)
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
|Int J Oncol. 2014 Nov;45(5):2085-91. |
|Identification of Hirsutine as an anti-metastatic phytochemical by targeting NF-κB activation.[Pubmed: 25175557 ]|
|Nuclear factor-κB (NF-κB) activation has been implicated not only in carcinogenesis but also in cancer cell invasion and metastatic process; therefore, targeting the NF-κB pathway is an attractive strategy for controlling meta-stasis.
METHODS AND RESULTS:
Amongst 56 chemically defined compounds derived from natural products, we have identified a new phytochemical compound Hirsutine, which strongly suppresses NF-κB activity in murine 4T1 breast cancer cells. In accordance with the NF-κB inhibition, Hirsutine reduced the metastatic potential of 4T1 cells, as seen in the inhibition of the migration and invasion capacity of 4T1 cells. Hirsutine further inhibited the constitutive expression of MMP-2 and MMP-9 in 4T1 cells, and reduced the in vivo lung metastatic potential of 4T1 cells in the experimental model.
Given that the migration of human breast cancer cells was also inhibited, our present study implies that Hirsutine is an attractive phytochemical compound for reducing metastasis potential of cancer cells by regulating tumor-promoting NF-κB activity.
|PLoS One. 2015 Apr 24;10(4):e0119477. |
|The novel analogue of hirsutine as an anti-hypertension and vasodilatary agent both in vitro and in vivo.[Pubmed: 25909998]|
METHODS AND RESULTS:
In this paper, an analogue of Hirsutine (compound 1) has been synthesized and evaluated as an anti-hypertension agent, which exhibits extraordinary effects on the contractile response of thoracic aorta rings from male SD rats in vitro (IC50 = 1.129×10(-9)±0.5025) and the abilities of reducing the systolic blood pressure (SBP) and heart rate (HR) of SHR in vivo. The mechanism investigation reveals that the vasodilatation induced by compound 1 is mediated by both endothelium-dependent and -independent manners. The relaxation in endothelium-intact aortic rings induced by compound 1 can be inhibited by L-NAME (1×10(-6) mol•L(-1)) and ODQ (1×10(-6) mol•L(-1)). Moreover, compound 1 can also block Ca2+ influx through L-type Ca2+ channels and inhibit intracellular Ca2+ release while no effect on K+ channel has been observed.
All these data demonstrated that the NO/cyclic GMP pathway can be involved in endothelium-dependent manner induced by compound 1. Meanwhile the mechanism on the vasodilatation of compound 1 probably also related to blockade of Ca2+ influx through L-type Ca2+ channels and inhibition of intracellular Ca2+ release may have no relationship with K+ channels.