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Ligustrazine Hydrochloride
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name Ligustrazine Hydrochloride
Price: $30 / 20mg
CAS No.: 76494-51-4
Catalog No.: CFN99910
Molecular Formula: C8H12N2.HCl
Molecular Weight: 208.69 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Source: The rhizomes of Ligusticum chuanxiong Hort.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
Size /Price /Stock 10 mM * 1 mL in DMSO / $8.9 / In-stock
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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: Ligustrazine hydrochloride has antithrombotic effect, has certain protection effect on the vascular endothelium undergoing cardiopulmonary bypass (CPB), and can inhibit the activation of humai platelet following severe brain injury , improve t'ie balance, of TXA2 - PGI2 within the circulatory blood. It can exert down-regulate effects on Colon26 secretion of immunosuppressors and its tumor immunosuppression.
Targets: IL Receptor | NOS | NO | TGF-β/Smad | TXA2 - PGI2 | VEGFR
In vitro:
Chinese Journal of Immunology, 2009, 25(5):413-6.
Study on the down-regulatory effects of Ligustrazine Hydrochloride on tumor-induced immunosuppression by Colon26 tumor cells in vitro[Reference: WebLink]
To study the regulatory effects of Ligustrazine Hydrochloride(LHC)on tumor-induced immunosuppression by Colon26 cells in vitro.
METHODS AND RESULTS:
Colon26 cells were cultured for 48 h in the presense of LHC and either the cell fraction or the cultural supernatants was collected,with the untreated Colon26 cells as control for the study.The down-regulating effects of LHC on tumor immunosuppressions (including the suppressed NK killing and ConA induced transformation of murine spleen cells detected by MTT,and the reduced expression levels of IL-2Rα,CD3ε+ζ+ and CD3ε-ζ+ detected by FCM) were determined.The concentrations of immunosuppressive cytokines,including TGF-β1,VEGF,IL-4,IL-6 and IL-10,in the supernatants were analyzed by quantitative ELISA.The relationship among the down-regulatory effects of LHC on secretion immunosuppressive cytokines and tumor immunosuppressions were evaluated by multiple linear regression analysis.All of the cytokines assayed were found in the supernatant of Colon26 treated without LHC,in which TGF-β1 was the highest,and the significant inhibition of five immune functions mentioned above was showed.To the Colon26 treated by LHC,the concentrations of TGF-β1,IL-6 and IL-10 in the first re-cultured supernatant and its inhibition of five immunol functions decreased greatly.The concentrations of TGF-β1 and IL-6 in the second re-cultured supernatant and its inhibitions of transformation,CD3+ζ+ and CD3-ζ+resumed highly.The positive correlations existed between TGF-β1 and inhibition of immunol functions except for transformation,between IL-6 and inhibition of transformation or CD3-ζ+,between IL-10 and inhibition of NK killing or IL-2Rα or CD3+ζ+,respectively.
CONCLUSIONS:
LHC can exert down-regulate effects on Colon26 secretion of immunosuppressors and its tumor immunosuppression.Reducing tumor immunosuppression of Colon26 through decreasing its secretion of immunosuppressors should be one of anti-tumor mechanisms of LHC.
In vivo:
Zhongguo Zhong Xi Yi Jie He Za Zhi. 2014 May;34(5):531-5.
[Effect of ligustrazine hydrochloride on coagulation reaction and inflammation reaction in single valve replacement patients with rheumatic heart disease undergoing cardiopulmonary bypass].[Pubmed: 24941838]
To observe the protection effect of Ligustrazine Hydrochloride (LH) on coagulation reaction and inflammation reaction in single valve replacement patients with rheumatic heart disease undergoing cardiopulmonary bypass (CPB).
METHODS AND RESULTS:
Totally 40 patients undergoing single valve replacement were recruited in the study and randomly assigned to the two groups, the treatment group and the control group, 20 in each group. In treatment group LH (3 mg/kg) was intravenously infused from the jugular vein. LH (3 mg/kg) was also added in the CPB priming. In the control group LH was replaced by equal amount of normal saline. Endothelial micro-particles (EMP) count was detected before CPB, 30 min after CPB, 1 h and 24 h after CPB finished. The coagulation reaction time (R), coagulation time (K), clotting formation velocity (alpha angle), maximum amplitude (MA), coagulation index (CI), platelet (PLT), hypersensitive C reactive protein (hs-CRP), IL-6, and IL-10 were detected before CPB, 1 h and 24 h after CPB finished. There was no statistical difference in aorta arresting time, period of CPB, post-operative drainage volume, plasma transfusion volume, post-operative respirator assistant time, and hospitalization time between the two groups (P >0.05). Compared with pre-CPB in the same group, the count of EMP was much higher at 30 min after CPB and 1 h after CPB finished (P < 0.01). R and K, hs-CRP, IL-6, and IL-10 increased at 1 h and 24 h after CPB finished (P <0.01,P < 0.05). The alpha angle,.MA, CI, and PLT decreased 1 h after CPB finished (P <0.01). The a angle increased, while CI and PLT decreased 24 h after CPB finished (P <0.05). Compared with the control group in the same period, the count of EMP was lower in the treatment group 30 min after CPB and 1 h after CPB finished (P <0. 05, P <0. 01). R and K values obviously decreased in treatment group 1 hour after CPB finished (P <0. 05), while a angle, MA, CI, and PLT increased (P <0. 05, P <0. 01). hs-CRP and IL-6 decreased in the treatment group 1 h and 24 h after CPB finished (P <0.05), while IL-10 increased (P <0.05). The count of PLT increased 24 h after CPB finished in the treatment group (P <0. 05).
CONCLUSIONS:
LH had certain protection effect on the vascular endothelium undergoing CPB, and lower excessive activation of coagulation reaction and inflammation reaction in patients undergoing CPB.
Chinese Journal of Nervous & Mental Diseases, 1994,20(3):151-4.
Effect of ligustrazine hydrochloride on the concentration of TXB2 and 6-Keto-PGF1a of the plasma and ventricular cerebrospinal fluid and intracranial pressure in severe brain injured patients.[Reference: WebLink]

METHODS AND RESULTS:
Twenty-eighht cases of brain injured patients were divided into two groups: treated with or with- out Ligustrazine Hydrochloride respectively. The concentration of TXBi and 6KP in plasma and V CSF were analysed with RIA before and 3 hours after the treatment, and ICP were also recorded at the same time. The result showed: before the treatment, the concentration of TXB2 and 6KP in plasma and VCSF in both groups were significantly higher than that of the controlled group, Ligustrazine Hydrochloride could reduce the concentration of TXB2 in plasma and VCSF and had no significant influence on ICP.
CONCLUSIONS:
These results suggest that Ligustrazine Hydrochloride can inhibit the activation of humai platelet following severe brain injury , improve t'ie balance, of TXA2 - PGI2 within the circulatory blood. It also implies that Ligustrazine Hydrochloride might be used as one of the agents to treat brain injury.
Ligustrazine Hydrochloride Description
Source: The rhizomes of Ligusticum chuanxiong Hort.
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 4.7918 mL 23.959 mL 47.918 mL 95.8359 mL 119.7949 mL
5 mM 0.9584 mL 4.7918 mL 9.5836 mL 19.1672 mL 23.959 mL
10 mM 0.4792 mL 2.3959 mL 4.7918 mL 9.5836 mL 11.9795 mL
50 mM 0.0958 mL 0.4792 mL 0.9584 mL 1.9167 mL 2.3959 mL
100 mM 0.0479 mL 0.2396 mL 0.4792 mL 0.9584 mL 1.1979 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:
Zhongguo Zhong Yao Za Zhi. 2012 Jun;37(12):1836-9.
[Protective effect of ligustrazine hydrochloride on homocysteine-injured ECV304 cells].[Pubmed: 22997835]
To detect the protective effect of Ligustrazine Hydrochloride on homocysteine-injured ECV304 cells.
METHODS AND RESULTS:
In the in vitro study, human umbilical vein endothelial cells were selected as objects, with homocysteine as the molding agent, to judge the injury degree by monitoring NOS and NO contents. Based on that, the best homocysteine concentration in ECV304 cells, the best reaction time could be determined, and an endothelial cell injury model was established. After adding Ligustrazine Hydrochloride, NOS and NO contents in injured endothelial cells were determined to observe the protective effect of Ligustrazine Hydrochloride. It was proved that the optimal concentration of homocysteine on injured ECV304 cell was 1 mmol x L(-1), the best reaction time was 48 h. An injured endothelial cell model was established. At the same time, positive drug nitroglycerin and Ligustrazine Hydrochloride displayed a protection effect on injured ECV304 cells, NOS and NO formation were significantly increased compared with the model group.
CONCLUSIONS:
Ligustrazine Hydrochloride has a protective effect on homocysteine-injured ECV304 cells. The model established in this study can be used to screen anti-myocardial ischemia drugs targeting at an endothelial cell protective agent.
Animal Research:
J Res Med Sci. 2013 Aug; 18(8): 704–706.
Antithrombotic effect of ligustrazine hydrochloride injection on the model of induced arteriovenous shunt thrombosis.[Pubmed: 24379848]
The objective of this study is to optimize the effective dose of heparin and Ligustrazine Hydrochloride injection (LHI) for drug combination.
METHODS AND RESULTS:
The animal clinical study of LHI was performed by the rat's model of induced arteriovenous shunt thrombosis. Experimental animals were grouped into several groups and separately treated with both LHI (20, 40, 80 mg/kg, i.p.) and heparin (60, 55, and 50 U/kg; 5000 U/ml; Sigma, i.v). The study had used thrombus weight, protein concentration in thrombus homogenate, inhibition rate of thrombosis, and plasma anti-thrombin activity as indications. The group combination (50, 80) got the result of 100% antithrombotic activity with 0 ± 0 mg of thrombus weight, 14 ± 3 μg/ml of protein concentration in thrombus homogenate and 1.5 ± 0.04 U/ml of plasma anti-thrombin activity. Its anti-thrombotic effect was much better than individual groups treated with LHI in a dose of 0 mg/kg and group of combination (0, 80) (P < 0.05) while antithrombotic effect of 55 and 60 U/kg heparin alone was only 37-58%. Therefore, the group of combination (50, 80) was optimal for 100% antithrombotic activity.
CONCLUSIONS:
Optimal combined doses of LHI and heparin preventing blood coagulation were determined and the results were available. It may give some hint for the further clinical application on human.
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