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Leonurine hydrochloride
Leonurine hydrochloride
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name Leonurine hydrochloride
Price: $50 / 20mg
CAS No.: 24735-18-0
Catalog No.: CFN99529
Molecular Formula: C14H21O5N3.HCl
Molecular Weight: 311.33 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Source: The herbs of Leonurus heterophyllus Sweet.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
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Biological Activity
Description: Leonurine hydrochloride has anti-oxidative, anti-inflammatory, and antitumor activities, it exerts antidiabetic, cardiovascular, and bovine mastitis protection, it has an inhibitory effect on bleeding caused by incomplete abortion. Leonurine hydrochloride increases the expression levels of caspase-3, caspase-9 and Bax/Bcl-2, and it inhibits osteoclastogenesis and prevent osteoporosis associated with estrogen deficiency by inhibiting the NF-κB and PI3K/Akt signaling pathways.
Targets: NF-kB | PI3K | Akt | IkB | ERK | p38MAPK | AP-1 | PKC | NO | Caspase | Bcl-2/Bax | ROS | Calcium Channel | IKK
In vitro:
Bone. 2015 Jun;75:128-37.
Leonurine hydrochloride inhibits osteoclastogenesis and prevents osteoporosis associated with estrogen deficiency by inhibiting the NF-κB and PI3K/Akt signaling pathways.[Pubmed: 25708053]
Osteoclasts, the primary bone resorbing cells, are responsible for destructive bone diseases such as postmenopausal osteoporosis, rheumatoid arthritis, and periodontitis. Many plant-derived traditional medicines that might suppress the formation and/or function of osteoclasts are promising treatments for osteoclast-related diseases.
METHODS AND RESULTS:
In this study, we investigated the effects of Leonurine hydrochloride (LH) on receptor activator NF-κB ligand (RANKL)-induced osteoclastogenesis and ovariectomy-induced bone loss. Leonurine hydrochloride is a synthetic chemical compound based on the structure of leonurine, which is found in motherwort and has been reported to exhibit phytoestrogenic activity. In RAW 264.7 cells and mouse bone marrow monocytes (BMMs), Leonurine hydrochloride suppressed RANKL-induced osteoclastogenesis and actin ring formation in a dose-dependent manner. Leonurine hydrochloride targeted RANKL-induced osteoclastogenesis and bone resorption at an early stage. Molecular analysis demonstrated that Leonurine hydrochloride attenuated RANKL-induced NF-κB signaling by inhibiting the phosphorylation and degradation of IκBα and NF-κB p65 nuclear translocation. Leonurine hydrochloride inhibited the RANK-TRAF6 association triggered by RANKL binding and the phosphatidylinositol 3-kinase (PI3K)/Akt axis, without significantly affecting the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) and AP-1 signaling pathways. Leonurine hydrochloride attenuated the RANKL-stimulated expression of osteoclast-related genes including NFATc1, tartrate resistant acid phosphatase (TRAP), cathepsin K, and osteoclast-associated receptor (OSCAR). Consistent with the in vitro results, Leonurine hydrochloride administration attenuated osteoclast activity, thus preventing bone loss caused by estrogen deficiency in mice. In this study, Leonurine hydrochloride suppressed RANKL-induced osteoclastogenesis via RANK-TRAF6, NF-κB, and PI3K/Akt signaling.
CONCLUSIONS:
These data provide the first evidence that Leonurine hydrochloride might be a promising therapeutic compound to treat osteoclast-related diseases, such as osteoporosis.
J Cell Physiol . 2019 May;234(5):6940-6950.
Inhibition of PI3K/Akt/NF-κB signaling with leonurine for ameliorating the progression of osteoarthritis: In vitro and in vivo studies[Pubmed: 30417459]
Abstract Osteoarthritis (OA) is characterized as the degeneration and destruction of articular cartilage. In recent decades, leonurine (LN), the main active component in medical and edible dual purpose plant Herba Leonuri, has been shown associated with potent anti-inflammatory effects in several diseases. In the current study, we examined the protective effects of LN in the inhibition of OA development as well as its underlying mechanism both in vitro and in vivo experiments. In vitro, interleukin-1 beta (IL-1β) induced over-production of prostaglandin E2, nitric oxide, inducible nitric oxide synthase, cyclooxygenase-2, interleukin-6 and tumor necrosis factor alpha were all inhibited significantly by the pretreatment of LN at a dose-dependent manner (5, 10, and 20 μM). Moreover, the expression of thrombospondin motifs 5 (ADAMTS5) and metalloproteinase 13 (MMP13) was downregulated by LN. All these changes led to the IL-1β induced degradation of extracellular matrix. Mechanistically, the LN suppressed IL-1β induced activation of the PI3K/Akt/NF-κB signaling pathway cascades. Meanwhile, it was also demonstrated in our molecular docking studies that LN had strong binding abilities to PI3K. In addition, LN was observed exerting protective effects in a surgical induced model of OA. To sum up, this study indicated LN could be applied as a promising therapeutic agent in the treatment of OA. Keywords: PI3K/Akt/NF-κB; leonurine (LN); osteoarthritis (OA).
In vivo:
Eur J Obstet Gynecol Reprod Biol. 2013 Jul;169(2):299-303.
Effect of leonurine hydrochloride on endothelin and the endothelin receptor-mediated signal pathway in medically-induced incomplete abortion in rats.[Pubmed: 23541415]
Endothelin (ET) is involved in uterine contractions. Our previous study showed that Leonurine hydrochloride (LH) inhibits abnormal bleeding caused by incomplete abortion through an increase in uterine contractions in rats. The present study was conducted to show that LH treatment regulates the ET-mediated signal pathway in abortion in rats.
METHODS AND RESULTS:
Early pregnancies in rats had incomplete abortions induced using mifepristone in combination with misoprostol. After the abortions, the rats were treated with LH orally for 7 days and surgery was performed. The sinistro-uterus was dissected for measurement of ET and nitric oxide (NO); the dextro-uterus was stored at -80°C for ET receptor (ETA and ETB) analysis. Myometrial cells from the dextro-uterus were cultured for measurement of phospholipase C (PLC) activity, intra-cellular Ca(2+) concentration ([Ca(2+)]i), and protein kinase C (PKC) activity. In in vivo experiments, LH treatment elevated the ET level and ET/NO ratio in rats with induced abortions and up-regulated ETA mRNA expression (P<0.01 vs. the model group), but there was no change in ETB mRNA. LH significantly increased the [Ca(2+)]i, PLC activity, and relative production of PKC protein in myometrial cells.
CONCLUSIONS:
LH increased uterine contractions in rats with incomplete abortions by modulating the ET receptor-mediated signal pathway.
Eur J Obstet Gynecol Reprod Biol. 2011 Dec;159(2):375-80.
Effects of leonurine hydrochloride on medically induced incomplete abortion in early pregnancy rats.[Pubmed: 22030073]
To determine the effect of Leonurine hydrochloride (LH) on abnormal bleeding induced by medical abortion.
METHODS AND RESULTS:
Rats had incomplete abortions induced in early pregnancy using mifepristone in combination with misoprostol. After abortion, rats were treated with Leonurine hydrochloride for 7 days, and the duration and volume of uterine bleeding were observed. Approximately 30min after the last treatment, the animals were killed and the uterine shape was observed. The sinistro-uteri were suspended in organ baths to record the contraction curves, including the frequency and tension for 10min; the dextro-uteri were fixed with formaldehyde for pathologic evaluation. In addition, blood samples were collected from the femoral artery for the measurement of estradiol (E₂) and progesterone (P) levels by radioimmunoassay. In in vivo experiments, compared with the model group, Leonurine hydrochloride treatment markedly reduced the volume of bleeding and intrauterine residual, and significantly shortened the duration of bleeding. From the contraction curve, Leonurine hydrochloride notably reinforced the frequency and tension of uterine contractions. Leonurine hydrochloride remarkably elevated the serum estradiol level in rats, but had no obvious effect on progesterone level.
CONCLUSIONS:
Leonurine hydrochloride has an inhibitory effect on bleeding caused by incomplete abortion; the mechanism may be related to up-regulation of the E₂ level, leading to an increase in uterine contractions and evacuation of intrauterine residuum.
Biomed Pharmacother . 2019 Feb;110:571-581.
Novel hepatoprotective role of Leonurine hydrochloride against experimental non-alcoholic steatohepatitis mediated via AMPK/SREBP1 signaling pathway[Pubmed: 30537674]
Abstract Background and aims: Non-alcoholic steatohepatitis (NASH) is the hepatic manifestation of metabolic syndrome and is characterized by steatosis, inflammation, and fibrosis. We aim to characterize the hepatoprotective effects of Leonurine hydrochloride (LH) and the possible pathway in a cell and rodent model of diet-induced steatohepatitis (NASH). Methods: For in vitro studies, Palmitic acid (PA) and free fatty acid (FFA) induced HepG2 and HL7702 steatosis cell models were used. For in vivo studies, NASH was induced by feeding mice MCD diet. These mice received either placebo or LH at three different doses (50、100、200 mg/kg/day) for 6 weeks. Histological staining's, and commercially available kits for ALT and AST and hepatic contents of TG, TC, MDA, SOD, and GSH were used to assess NASH. Furthermore, relative liver protein and gene expression levels were determined by Western Blot and qPCR, respectively. Results: After establishing NASH models, LH treatment improved lipid accumulation, hepatic contents of TG, TC, and expression levels of ALT and AST in dose-dependent manner. Also, LH improved MDA, SOD, and GSH expression levels. The results of RT-PCR and Western blotting showed that LH upregulated the expression of AMPK phosphorylation and downregulated SREBP-1c and its target genes expression level. Conclusions: Our data reveal the promising role of Leonurine hydrochloride in the prevention and treatment of NASH, in vitro and in vivo. This effect may be partially mediated by the AMPK/SREBP1 pathway. These findings provide a novel therapeutic target for the clinical treatment of NASH. Keywords: AMPK; Fibrosis; Inflammation; Leonurine; Non-alcoholic steatohepatitis; Steatosis.
Leonurine hydrochloride Description
Source: The herbs of Leonurus heterophyllus Sweet.
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: service@chemfaces.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.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 3.212 mL 16.0601 mL 32.1203 mL 64.2405 mL 80.3006 mL
5 mM 0.6424 mL 3.212 mL 6.4241 mL 12.8481 mL 16.0601 mL
10 mM 0.3212 mL 1.606 mL 3.212 mL 6.4241 mL 8.0301 mL
50 mM 0.0642 mL 0.3212 mL 0.6424 mL 1.2848 mL 1.606 mL
100 mM 0.0321 mL 0.1606 mL 0.3212 mL 0.6424 mL 0.803 mL
* 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.
Protocol
Cell Research:
Pharm Biol. 2015 Apr 9:1-7.
Leonurine hydrochloride induces apoptosis of H292 lung cancer cell by a mitochondria-dependent pathway.[Pubmed: 25856714]
Leonurine hydrochloride (LH), a major alkaloid compound extracted from Leonurus japonicas Houtt. (Labiatae), is considered to have antitumor roles. This study investigated its effects on human non-small cell lung cancer (NSCLC) H292 cells and illustrated the possible mechanism involved.
METHODS AND RESULTS:
After treatment with different concentrations of LH (0, 10, 25, and 50 μmol/L) for 6, 12, 24, 48, and 72 h, the cell viability was assessed by the MTT assay. After exposed to different doses of LH for 24 h, cell-cycle distribution, cell apoptosis, mitochondrial membrane potential (MMP), and reactive oxygen species (ROS) were monitored by flow cytometry. RT-PCR and western blot were used to detect the expression of apoptosis-related genes. LH significantly inhibited the proliferation of H292 cells in a time- and dose-dependent manner, and induced G0/G1 cell-cycle arrest. Coincidentally, LH treatment at a dose of 10, 25, and 50 μmol/L for 24 h increased apoptotic ratio from 4.9 ± 0.43% to 11.5 ± 1.12%, 19.3 ± 1.16%, and 61.3 ± 6.69%, respectively. The inhibition effect of LH on H292 cells was associated with the loss of MMP and the generation of ROS. The phosphorylation level of p38 was increased and Akt phosphorylation was reduced by LH treatment. Furthermore, LH treatment increased the expression levels of caspase-3, caspase-9 and Bax/Bcl-2.
CONCLUSIONS:
LH inhibits the proliferation and induces the apoptosis of H292 cells in a mitochondria-dependent pathway, and the specific mechanism need to be further explored.
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