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编 号：F169797
分子式：C52H74N16O15S2
分子量：1227.37
分子式：C52H74N16O15S2
分子量：1227.37
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CAS No: 14636-12-5
产品详情
生物活性：
Terlipressin is a vasopressin analogue with potent vasoactive properties. Terlipressin is a highly selective vasopressin V1 receptor agonist that reduces the splanchnic blood flow and portal pressure and controls acute variceal bleeding. Terlipressin exerts anti-inflammatory and anti-oxidative effects. Terlipressin has the potential for hepatorenal syndrome and norepinephrine-resistant septic shock research.
体内研究：
Using a mouse nonlethal hepatic ischemia-reperfusion (IR) model, Terlipressin administration significantly ameliorates IR-induced liver apoptosis, necrosis and inflammation.
体外研究：
Terlipressin (25 nM; 24-72 hours; IEC-6 cells) treatment significantly improves cell viability, proliferation and apoptosis in IEC-6 cells. Terlipressin inhibits the secretion of TNF-α and 15-F2t-isoprostane from IEC-6 cells following oxygen and glucose deprivation/re-oxygenation (OGD/R). Terlipressin administration following OGD attenuates OGD/R-induced cell damage via the PI3K signaling pathway.
Terlipressin is a vasopressin analogue with potent vasoactive properties. Terlipressin is a highly selective vasopressin V1 receptor agonist that reduces the splanchnic blood flow and portal pressure and controls acute variceal bleeding. Terlipressin exerts anti-inflammatory and anti-oxidative effects. Terlipressin has the potential for hepatorenal syndrome and norepinephrine-resistant septic shock research.
体内研究：
Using a mouse nonlethal hepatic ischemia-reperfusion (IR) model, Terlipressin administration significantly ameliorates IR-induced liver apoptosis, necrosis and inflammation.
体外研究：
Terlipressin (25 nM; 24-72 hours; IEC-6 cells) treatment significantly improves cell viability, proliferation and apoptosis in IEC-6 cells. Terlipressin inhibits the secretion of TNF-α and 15-F2t-isoprostane from IEC-6 cells following oxygen and glucose deprivation/re-oxygenation (OGD/R). Terlipressin administration following OGD attenuates OGD/R-induced cell damage via the PI3K signaling pathway.
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