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DL-Propargyl Glycine (hydrochloride) Sale

(Synonyms: PAG) 目录号 : GC43492

An irreversible inhibitor of H2S synthesis

DL-Propargyl Glycine (hydrochloride) Chemical Structure

Cas No.:16900-57-5

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1mg
¥199.00
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5mg
¥898.00
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10mg
¥1,597.00
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50mg
¥6,985.00
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产品描述

Hydrogen sulphide (H2S), a naturally occurring gasotransmitter, is a potent vasodilator and pro-inflammatory mediator. DL-Propargyl glycine (PAG) is an irreversible inhibitor of the H2S synthesizing enzyme cystathionine-γ-lyase (CSE). PAG blocks H2S synthesis activity in rat liver preparations with an IC50 value of 55 µM and abolishes the rise in plasma H2S in anaesthetized rats induced with hemorrhagic shock. At concentrations ranging from 25-100 mg/kg, PAG can reduce H2S-associated inflammation in rodent models of pancreatitis, oedema, and endotoxemia.

Chemical Properties

Cas No. 16900-57-5 SDF
别名 PAG
Canonical SMILES NC(C(O)=O)CC#C.Cl
分子式 C5H7NO2•HCl 分子量 149.6
溶解度 DMF: 20 mg/ml,DMSO: 20 mg/ml,Ethanol: 20 mg/ml,PBS (pH 7.2): 10 mg/ml 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 6.6845 mL 33.4225 mL 66.8449 mL
5 mM 1.3369 mL 6.6845 mL 13.369 mL
10 mM 0.6684 mL 3.3422 mL 6.6845 mL
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Research Update

Hydrogen sulfide impacts on inflammation-induced adipocyte dysfunction

Food Chem Toxicol 2019 Sep;131:110543.PMID:31154084DOI:10.1016/j.fct.2019.05.051.

A dual role of hydrogen sulfide (H2S) in inflammation is well-reported and recent studies demonstrated adipogenic effects of H2S in 3T3-L1 cells. Here, we aimed to investigate the effects of H2S on adipocyte differentiation and inflammation. H2S concentration in 3T3-L1 culture media was increased during adipocyte differentiation in parallel to adipogenic and Cth gene expression, and its inhibition using DL-Propargyl Glycine (PPG) impaired 3T3-L1 differentiation. GYY4137 and Na2S administration only in the first or in the last stage of adipocyte differentiation resulted in a significant increased expression of adipogenic genes. However, when GYY4137 or Na2S were administrated during all process no significant effects on adipogenic gene expression were found, suggesting that excessive H2S administration might exert negative effects on adipogenesis. In fact, continuous addition of Na2S, which resulted in Na2S excess, inhibited adipogenesis, whereas time-expired Na2S had no effect. In inflammatory conditions, GYY4137, but not Na2S, administration attenuated the negative effects of inflammation on adipogenesis and insulin signaling-related gene expression during adipocyte differentiation. In inflamed adipocytes, Na2S administration enhanced the negative effects of inflammatory process. Altogether these data showed that slow-releasing H2S improved adipocyte differentiation in inflammatory conditions, and that H2S proadipogenic effects depend on dose, donor and exposure time.

Inhibition of cystathionine gamma-lyase and the biosynthesis of endogenous hydrogen sulphide ameliorates gentamicin-induced nephrotoxicity

Eur J Pharmacol 2012 Jun 15;685(1-3):165-73.PMID:22546230DOI:10.1016/j.ejphar.2012.04.030.

Clinical use of gentamicin over prolonged periods is limited because of dose- and time-dependent nephrotoxicity. Primarily, lysosomal phospholipidosis, intracellular oxidative stress and heightened inflammation have been implicated. Hydrogen sulphide is an endogenously produced signal transduction molecule with strong anti-inflammatory, anti-apoptotic and cytoprotective properties. In several models of inflammatory disease however, tissue damage has been associated with increased activity of cystathionine gamma-lyase, biosynthesis of hydrogen sulphide and activation of leukocytes. The aim of this study was to determine effects of inhibiting hydrogen sulphide biosynthesis by DL-Propargyl Glycine (an irreversible inhibitor of cystathionine gamma-lyase) on inflammation, necrosis and renal function, following treatment with gentamicin in rats. Adult female Sprague-Dawley rats were divided into six groups and treated with; physiological saline, sodium hydrosulphide, DL-Propargyl Glycine, gentamicin, a combination of gentamicin and sodium hydrosulphide, or gentamicin and DL-Propargyl Glycine respectively. Gentamicin-induced histopathological changes including inflammatory cell infiltration and tubular necrosis were attenuated by co-administering gentamicin with DL-Propargyl Glycine (P<0.05 compared to saline controls and P<0.05 compared to gentamicin only). Similarly, DL-Propargyl Glycine caused a significant reduction (P<0.05) in lipid peroxidation, production of superoxide and the activation of tumour necrosis factor-alpha in gentamicin-treated animals. These data show that protective effects of DL-Propargyl Glycine might be related at least in part, to the reduced inflammatory responses observed in animals treated with both gentamicin and DL-Propargyl Glycine. Thus, enzyme systems involved in hydrogen sulphide biosynthesis may offer a viable therapeutic target in alleviating the nephrotoxic effects of gentamicin.

Hydrogen sulfide ameliorates cardiovascular dysfunction induced by cecal ligation and puncture in rats

Hum Exp Toxicol 2015 Oct;34(10):953-64.PMID:25791320DOI:10.1177/0960327114564794.

Hydrogen sulfide (H2S) is an endogenously produced gaseous messenger that participates in regulation of cardiovascular functions. This study evaluates the possible protective effect of H2S in cardiovascular dysfunction induced by cecal ligation and puncture (CLP) in rats. After 24 h of induction of CLP, heart rate (HR), mortality, cardiac and inflammation biomarkers (creatine kinase-MB (CK-MB) isozyme, cardiac troponin I (cTnI), C-reactive protein (CRP), and lactate dehydrogenase (LDH)), in vitro vascular reactivity, histopathological examination, and oxidative biomarkers (malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD)) were determined. CLP induced elevations in HR, mortality, serum CK-MB, cTnI, CRP, and LDH, in addition to impaired aortic contraction to potassium chloride and phenylephrine and relaxation to acetylcholine without affecting sodium nitroprusside responses. Moreover, CLP increased cardiac and aortic MDA and decreased SOD, without affecting GSH and caused a marked subserosal and interstitial inflammation in endocardium. Sodium hydrosulfide, but not the irreversible inhibitor of H2S synthesis DL-Propargyl Glycine, protected against CLP-induced changes in HR, mortality, cardiac and inflammatory biomarkers, oxidative stress, and myocardium histopathological changes without affecting vascular dysfunction. Our results confirm that H2S can attenuate CLP-induced cardiac, but not vascular, dysfunction possibly through its anti-inflammatory and antioxidant effects.

Role of hydrogen sulfide in hepatic ischemia-reperfusion-induced injury in rats

Liver Transpl 2009 Oct;15(10):1306-14.PMID:19790158DOI:10.1002/lt.21810.

Hydrogen sulfide (H2S) displays anti-inflammatory and cytoprotective activities as evidenced by the inhibition of myocardial ischemia-reperfusion injury and production of lipid peroxidation. H2S also exerts many physiological or pathological effects on livers. Therefore, we designed the present study to investigate the roles of H2S in hepatic ischemia-reperfusion (HIR)-induced injury in rats by measuring H2S levels, H2S synthesizing activity, and cystathionine gamma-lyase (CSE) messenger RNA (mRNA) expression. We also applied DL-Propargyl Glycine (PAG) and sodium hydrosulfide (NaHS) to investigate their effects on the severity of liver injury induced by HIR. The levels of H2S, H2S production activity, and CSE mRNA expression in livers were increased by HIR. Administration of NaHS significantly attenuated the severity of liver injury and inhibited the production of lipid peroxidation, serum inflammatory factors [including nitric oxide, tumor necrosis factor alpha (TNF-alpha), interleukin 10, and intercellular cell adhesion molecule 1], cell apoptosis, and apoptosis-related proteins (including caspase-3, Fas, Fas ligand, and TNF-alpha), which were caused or elevated by HIR, whereas PAG aggravated them. However, NaHS or PAG did not show significant effects on the activation of caspase-9, which was also increased by HIR. Although further investigation is required, this study may indicate that H2S plays a protective role in HIR-induced injury.

Cystathionine gamma-lyase of perivascular adipose tissue with reversed regulatory effect in diabetic rat artery

Biotechnol Biotechnol Equip 2015 Jan 2;29(1):147-151.PMID:26019628DOI:10.1080/13102818.2014.991565.

The aim of this study is to reveal the regulatory role of cystathionine gamma-lyase (CSE), the main source of hydrogen sulphide (H2S) in perivascular adipose tissue (PVAT), of diabetic rats. Diabetes was induced in male rats by a single intraperitoneal injection of streptozotocin. Animals with glucose levels above 20 mmol/L were determined as diabetic. The rat gracilis arteries (a. gracilis) were dissected with or without PVAT. In all in vitro experiments endothelium-denuded preparations were used for isometric contraction measurements. Increasing concentrations of 5-hydroxytryptamine (5-HT) from 10-10 to 10-5 mol/L were applied to induce gradual increase in force of contractions of circular artery segments. The relaxing effect of CSE was inhibited by DL-Propargyl Glycine (PGG). The presence of PVAT decreases the contractile response to 5-HT of a. gracilis from control rats. This response is reversed in contraction studies in the same rat artery from diabetic rats. DL-PPG (1 mmol/L) induced significant increase of the force of contraction in artery preparations with PVAT from control rats in the whole range of 5-HT. In contrast, PGG had a relaxing effect in high concentrations of 5-HT (10-6 and 10-5 mol/L) in diabetic rat arteries with PVAT. It is concluded that in skeletal muscle artery from diabetic rats, a mediator related to H2S is released from PVAT. This paracrine mediator increases the maximal force of contraction of endothelium-denuded preparations at higher concentrations of 5-HT.