| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 200mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
Cell lines | HepaRG hepatocytes and HSECs |
Preparation Method | HSECs were treated with different concentrations of retrorsine, crotaline (monocrotaline) or clivorine dissolved in ECM containing DMSO (0.5% final concentration) or ECM containing 0.5% DMSO as solvent controls in two-layer transwell co-culture model for 24 h. |
Reaction Conditions | 100-1200uM,24h |
Applications | In the absence of HepaRG hepatocytes, even at significantly high concentration (1200 μM) for 24 h treatment, Crotaline did not affect viability of HSECs, indicating no cytotoxicity. In contrast, after 24 h treatment in the two-layer transwell co-culture model with co-culture of HSECs and HepaRG hepatocytes, significant decrease in HSEC viability in a concentration-dependent manner was observed for Crotaline. |
Animal models | 20 male Sprague Dawley rats (SD; 220-270g) |
Preparation Method | Control group received vehicle for crotaline. Pre-pulmonary hypertension (PH) group received a single injection of Crotaline to induce and were sacrificed after 14 days. |
Dosage form | A single injection crotaline 60 mg/kg for 14 days |
Applications | Changes in multiple pathways associated with PH development were observed by crotaline injection, including activated glycolysis, increased proliferation markers, disruption of carnitine homeostasis, increased inflammatory and fibrotic biomarkers, and decreased glutathione biosynthesis. |
| 产品描述 | Crotaline is an pyrrolizidine alkaloid extracted from the seeds of the Crotalaria spectabilis plant to induce pulmonary vascular syndrome in rats[1]. crotaline a natural ligand exhibits dose-dependent cytotoxicity with potent antineoplastic activity. The in vitro cytotoxicity of crotaline is proved at IC50 24.966 μg/mL and genotoxicity at 2 X IC50 against HepG2 cells[2]. In the absence of HepaRG hepatocytes, even at significantly high concentration (1200 μM) for 24 h treatment, Crotaline did not affect viability of HSECs, indicating no cytotoxicity. In contrast, after 24 h treatment in the two-layer transwell co-culture model with co-culture of HSECs and HepaRG hepatocytes, significant decrease in HSEC viability in a concentration-dependent manner was observed for Crotaline[8]. Crotaline causes pulmonary vascular syndrome in rats, characterized by proliferative pulmonary vasculitis, pulmonary hypertension (PH), and cor pulmonale[3].Changes in multiple pathways associated with PH development were observed by crotaline injection, including activated glycolysis, increased proliferation markers, disruption of carnitine homeostasis, increased inflammatory and fibrotic biomarkers, and decreased glutathione biosynthesis[5].Using rats (14 days after exposure to crotaline), changes in multiple pathways associated with the development of PH, including activated glycolysis, increased markers of proliferation, disruptions in carnitine homeostasis, increased inflammatory and fibrosis biomarkers, and a reduction in glutathione biosynthesis[4].PAH induced by Crotaline is a progressive disease with persistent inflammation. The inflammation in Crotaline -PAH model includes acute (the first 6 days after Crotaline injection) and chronic stages (after acute inflammation stage). Acute inflammation stage may be the time window of anti-inflammatory treatment in PAH induced by Crotaline[6,7]. References: |
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