ClivorineCAS# 33979-15-6 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 33979-15-6 | SDF | Download SDF |
| PubChem ID | 21606566 | Appearance | Cryst. |
| Formula | C21H27NO7 | M.Wt | 405.45 |
| Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| SMILES | CC1C=C(C(=O)OC2CC[N+]3(C2(C(=CC3)COC(=O)C1(C)OC(=O)C)[O-])C)C=C | ||
| Standard InChIKey | YEGVHSDONMXATH-LKVOMWJFSA-N | ||
| Standard InChI | InChI=1S/C21H27NO7/c1-6-15-11-13(2)20(4,29-14(3)23)19(25)27-12-16-7-9-22(5)10-8-17(21(16,22)26)28-18(15)24/h6-7,11,13,17H,1,8-10,12H2,2-5H3/b15-11-/t13-,17+,20-,21?,22?/m0/s1 | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | 1. Clivorine has anti-proliferative function in L-02 cells may be due to its inducing cell apoptosis with independent of p53 protein. 2. Clivorine itself has direct toxicity on HEK293 cells, and phosphorylated JNK may play some role in counteracting the toxicity of Clivorine on HEK293 cells. 3. Clivorine induces hepatotoxicity and acute liver injury, which can be protected by quercetin, trolox and epidermal growth factor via inhibiting apoptotic cell death and ameliorating oxidative stress injury. |
| Targets | EGFR | Caspase | JNK | ERK |
Clivorine Dilution Calculator
Clivorine Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4664 mL | 12.332 mL | 24.664 mL | 49.3279 mL | 61.6599 mL |
| 5 mM | 0.4933 mL | 2.4664 mL | 4.9328 mL | 9.8656 mL | 12.332 mL |
| 10 mM | 0.2466 mL | 1.2332 mL | 2.4664 mL | 4.9328 mL | 6.166 mL |
| 50 mM | 0.0493 mL | 0.2466 mL | 0.4933 mL | 0.9866 mL | 1.2332 mL |
| 100 mM | 0.0247 mL | 0.1233 mL | 0.2466 mL | 0.4933 mL | 0.6166 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Pyrrolizidine alkaloid clivorine induced oxidative injury on primary cultured rat hepatocytes.[Pubmed:20144959]
Hum Exp Toxicol. 2010 Apr;29(4):303-9.
Clivorine is an otonecine-type hepatotoxic pyrrolizidine alkaloid (HPAs), to which humans are exposed when consuming herbs containing such components. In the present study, we investigated Clivorine-induced oxidative stress injury on primary cultured rat hepatocytes. Rat hepatocytes were treated with various concentrations of Clivorine (1-100 microM) for 48 hours, and then cell viability was detected by 3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay, while lipid peroxidation (LPO) level, glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) activities were determined to evaluate the oxidative injury. The results of MTT assay showed that Clivorine decreased cell viability in a concentration-dependent manner. Clivorine also increased LPO amounts in rat hepatocytes at the concentrations of 50 microM and 100 microM. Further results showed that Clivorine decreased GPx, GST and GR activities, which are all reduced glutathione (GSH)-related antioxidant enzymes. CAT and SOD are both important antioxidant enzymes, and the results showed that Clivorine increased CAT activity at the low concentration of 5 muM and decreased cellular SOD activity at all concentrations. Taken together, our results demonstrated that Clivorine induced toxicity on primary cultured rat hepatocytes by causing the damage on cellular redox balance.
The toxic effect of pyrrolizidine alkaloid clivorine on the human embryonic kidney 293 cells and its primary mechanism.[Pubmed:18249102]
Exp Toxicol Pathol. 2008 Jun;60(1):87-93.
Clivorine is an otonecine-type pyrrolizidine alkaloid (PA) isolated from the Chinese medicinal plant Ligularia hodgsonii Hook., and our previous reports have shown its toxicity on human normal liver L-02 cells. It is generally believed that biotransformation of PAs to its metabolites is required for their toxicity; thus, there is nearly no report about the toxicity of Clivorine on other non-hepatic cells in vitro. The aim of this study is to observe the toxicity of Clivorine on the non-hepatic human embryonic kidney 293 (HEK293) cell that is of epithelial origin, and its primary mechanism. Our results showed that Clivorine significantly reduced HEK293 cell viability, but there was no detectable apoptotic DNA ladder and cleaved fragments of caspase-3 and caspase-9 in Clivorine-treated cells, which indicates the toxicity of Clivorine is not due to inducing apoptosis. The results of western blot showed that Clivorine induced sustained p38, c-Jun N-terminal kinase (JNK) and extracellular signal-related kinases (ERK1/2) phosphorylation in a concentration- and time-dependent manner, and the JNK inhibitor SP600125 significantly augmented the toxicity of Clivorine. Our results suggest that Clivorine itself has direct toxicity on HEK293 cells, and phosphorylated JNK may play some role in counteracting the toxicity of Clivorine on HEK293 cells.
Quercetin prevents pyrrolizidine alkaloid clivorine-induced liver injury in mice by elevating body defense capacity.[Pubmed:24905073]
PLoS One. 2014 Jun 6;9(6):e98970.
Quercetin is a plant-derived flavonoid that is widely distributed in nature. The present study is designed to analyze the underlying mechanism in the protection of quercetin against pyrrolizidine alkaloid Clivorine-induced acute liver injury in vivo. Serum transaminases, total bilirubin analysis, and liver histological evaluation demonstrated the protection of quercetin against Clivorine-induced liver injury. Terminal dUTP nick end-labeling assay demonstrated that quercetin reduced the increased amount of liver apoptotic cells induced by Clivorine. Western-blot analysis of caspase-3 showed that quercetin inhibited the cleaved activation of caspase-3 induced by Clivorine. Results also showed that quercetin reduced the increase in liver glutathione and lipid peroxidative product malondialdehyde induced by Clivorine. Quercetin reduced the enhanced liver immunohistochemical staining for 4-hydroxynonenal induced by Clivorine. Results of the Mouse Stress and Toxicity PathwayFinder RT2 Profiler PCR Array demonstrated that the expression of genes related with oxidative or metabolic stress and heat shock was obviously altered after quercetin treatment. Some of the alterations were confirmed by real-time PCR. Our results demonstrated that quercetin prevents Clivorine-induced acute liver injury in vivo by inhibiting apoptotic cell death and ameliorating oxidative stress injury. This protection may be caused by the elevation of the body defense capacity induced by quercetin.
Protection of epidermal growth factor against clivorine-induced mitochondrial-mediated apoptosis in hepatocytes.[Pubmed:19437449]
Environ Toxicol. 2010 Jun;25(3):304-9.
Pyrrolizidine alkaloids (PAs) are well-known natural hepatotoxins. In this study, we investigated the protection of epidermal growth factor (EGF) against the hepatotoxicity of Clivorine, which is an otonecine-type PA from traditional Chinese medicine Ligularia hodgsonii Hook. Cell viability assay and cell morphology observation showed that EGF (1 ng/mL) reversed Clivorine-induced cytotoxicity on human normal liver L-02 cells. EGF (1 ng/mL) also inhibited Clivorine-induced DNA fragmentation and caspase-3 cleavage. Our previous study has showed that antiapoptotic Bcl-xL degradation and mitochondrial-mediated apoptosis was involved in Clivorine-induced hepatotoxicity. In this study, we found that EGF (1 ng/mL) inhibited Clivorine-induced antiapoptotic Bcl-xL protein decrease, caspase-9 activation, and release of cytosolic cytochrome C. We further investigated the effects of vascular epidermal growth factor, basic fibroblast growth factor, and insulin-like growth factor-1 on Clivorine-induced cytotoxicity, and there is no significant protection observed. Our results suggest that EGF exerts its protective effects against Clivorine-induced hepatotoxicity probably by modulating mitochondrial-mediated apoptotic signal pathway.
Pyrrolizidine alkaloid clivorine-induced oxidative stress injury in human normal liver L-02 cells.[Pubmed:22495657]
Drug Discov Ther. 2009 Dec;3(6):247-51.
Clivorine is an otonecine-type pyrrolizidine alkaloid isolated from the traditional Chinese medicine Ligularia hodgsonii Hook. Pyrrolizidine alkaloids (PAs) are well-known hepatotoxins widely distributed around the world. The present study sought to evaluate Clivorineinduced oxidative injury in human normal liver L-02 cells. After cells were treated with various concentrations of Clivorine for 48 h, cellular total antioxidant capacity, glutathione-S-transferase (GST) and glutathione reductase (GR) were determined to evaluate oxidative injury. Results showed that cellular total antioxidant capacity and GST activity both increased in Clivorine-treated L-02 cells, while Clivorine decreased GR activity in cells. Further, the protective effects of some antioxidants such as ascorbic acid (vitamin C, Vc), Trolox, dithiothreitol (DTT) and mannitol against Clivorine-induced cytotoxicity were observed. Results showed that Trolox, which is an analogue of tocopherol (vitamin E, Ve), prevented Clivorine-induced cytotoxicity in L-02 cells. Taken together, these results revealed Clivorineinduced oxidative injury in human liver L-02 cells. These results also indicated the possible use of Trolox in the reduction of Clivorine-induced hepatotoxicity.
