产品
编 号：F318111
分子式：C215H347N61O65S
分子量：4858.49
分子式：C215H347N61O65S
分子量：4858.49
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
结构图
CAS No: 320367-13-3
产品详情
生物活性：
Lixisenatide is a GLP-1 receptor agonist. Lixisenatide inhibits the inflammatory response through down regulation of proinflammatory cytokines, and blocks of cellular signaling pathways. Lixisenatide decreases atheroma plaque size and instability in Apoe?/? Irs2+/? mice by reprogramming macrophages towards an M2 phenotype, which leads to reduced inflammation.
体内研究：
Lixisenatide (10 μg/kg，皮下注射， 一天一次持续一个月) 可减轻动脉粥样硬化负荷，产生更稳定的斑块。Lixisenatide (10 μg/kg，皮下注射， 一天一次持续一个月) 减少系统性炎症在给予致动脉粥样硬化饮食的 Apoe?/? Irs2+/? 小鼠中。Lixisenatide (1 nmol/kg，腹腔注射， 一天一次，连续 14 天 ) 在小剂量处理后对实验性早期糖尿病肾病具有肾脏保护作用。Animal Model:Apoe?/? Irs2+/? mice
Dosage:10 μg/kg
Administration:Subcutaneous injection (s.c.)
Result:Exhibited smaller atheromas in the aortic arch region.Reduced the lesion size in cross-sections of hearts.
Animal Model:Diabetic rats
Dosage:1 nmol/kg
Administration:Intraperitoneal injection (i.p.)
Result:Showed a significant amelioration on the elevated renal parameters. Showed significant mitigation in renal MDA and total NOx? (by 50.3 and 79.9%, respectively) and 43.9% elevation in renal total antioxidant capacity. Averted the observed increments in iNOS and COX-2 expressions in the renal tissues of the diabetic group.Decreased the level of TGF-β protein expression.
体外研究：
Lixisenatide (100 μM, 24 h) 抑制 Aβ25-35 诱导的海马细胞毒性。Lixisenatide (100 μM, 24 h) 缓解 Aβ25-35 对海马细胞 Akt-MEK1/2 信号通路的抑制作用。 Lixisenatide (10-20 μM, 48 h) 改善 IL-1β 诱导的氧化应激、线粒体功能障碍和成纤维样滑膜细胞凋亡。Lixisenatide (10-20 μM, 48 h) 减少 IL-1β 诱导 MMPs 的表达,并抑制了在成纤维样滑膜细胞中 IL-1β 的促炎通路的激活。Lixisenatide (10-20 μM, 6 h) 减少氧糖剥夺/再灌注诱导的人脐血管内皮细胞 ROS 生成。
Lixisenatide is a GLP-1 receptor agonist. Lixisenatide inhibits the inflammatory response through down regulation of proinflammatory cytokines, and blocks of cellular signaling pathways. Lixisenatide decreases atheroma plaque size and instability in Apoe?/? Irs2+/? mice by reprogramming macrophages towards an M2 phenotype, which leads to reduced inflammation.
体内研究：
Lixisenatide (10 μg/kg，皮下注射， 一天一次持续一个月) 可减轻动脉粥样硬化负荷，产生更稳定的斑块。Lixisenatide (10 μg/kg，皮下注射， 一天一次持续一个月) 减少系统性炎症在给予致动脉粥样硬化饮食的 Apoe?/? Irs2+/? 小鼠中。Lixisenatide (1 nmol/kg，腹腔注射， 一天一次，连续 14 天 ) 在小剂量处理后对实验性早期糖尿病肾病具有肾脏保护作用。Animal Model:Apoe?/? Irs2+/? mice
Dosage:10 μg/kg
Administration:Subcutaneous injection (s.c.)
Result:Exhibited smaller atheromas in the aortic arch region.Reduced the lesion size in cross-sections of hearts.
Animal Model:Diabetic rats
Dosage:1 nmol/kg
Administration:Intraperitoneal injection (i.p.)
Result:Showed a significant amelioration on the elevated renal parameters. Showed significant mitigation in renal MDA and total NOx? (by 50.3 and 79.9%, respectively) and 43.9% elevation in renal total antioxidant capacity. Averted the observed increments in iNOS and COX-2 expressions in the renal tissues of the diabetic group.Decreased the level of TGF-β protein expression.
体外研究：
Lixisenatide (100 μM, 24 h) 抑制 Aβ25-35 诱导的海马细胞毒性。Lixisenatide (100 μM, 24 h) 缓解 Aβ25-35 对海马细胞 Akt-MEK1/2 信号通路的抑制作用。 Lixisenatide (10-20 μM, 48 h) 改善 IL-1β 诱导的氧化应激、线粒体功能障碍和成纤维样滑膜细胞凋亡。Lixisenatide (10-20 μM, 48 h) 减少 IL-1β 诱导 MMPs 的表达,并抑制了在成纤维样滑膜细胞中 IL-1β 的促炎通路的激活。Lixisenatide (10-20 μM, 6 h) 减少氧糖剥夺/再灌注诱导的人脐血管内皮细胞 ROS 生成。
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