产品
编 号：F024252
分子式：C17H17NO3
分子量：283.32
分子式：C17H17NO3
分子量：283.32
产品类型
规格
价格
是否有货
5mg
询价
询价
10mg
询价
询价
25mg
询价
询价
50mg
询价
询价
结构图
CAS No: 105955-01-9
产品详情
生物活性：
KS370G is an orally active hypoglycemic and cardiovascular protective agent. KS370G improves left ventricular hypertrophy and function in pressure-overload mice heart. KS370G reduces renal obstructive nephropathy.
体内研究：
KS370G (1 mg/kg; oral; once daily for 8 weeks) 通过降低压力过载小鼠心脏 ERK、AKT 和 GSK3β 的磷酸化，改善左心室功能，抑制心脏肥厚。 KS370G (10 mg/kg; oral; once daily for 13 days) 通过减少小鼠炎症和氧化应激减轻单侧输尿管梗阻引起的肾纤维化。Animal Model:Pressure-overload ICR mice model
Dosage:1 mg/kg
Administration:Oral gavage, once daily for 8 weeks
Result:Inhibited cardiac hypertrophy and improved cardiac function induced by pressure overload. Decreased the plasma levels of atrial natriuretic peptide and lactate dehydrogenase. Significantly reduced pressure overload-induced increase of α-SMA and phosphorylation of ERK, AKT and GSK3β. Reduced cardiac collagen accumulation.
Animal Model:Male ICR mice, unilateral ureteral obstruction (UUO) model
Dosage:10 mg/kg
Administration:Oral, once daily for 13 days
Result:Significantly attenuated collagen deposition in the obstructed kidney and inhibited UUO-induced renal fibrosis markers expression, including fibronectin, type I collagen, vimentin, and α-smooth muscle actin (α-SMA). Significantly lowered the expression of renalinflammatory chemokines/adhesion molecules and monocyte cells marker (MCP-1, VCAM-1, ICAM-1 and CD11b). Reduced renal malondialdehyde levels and reversed the expression of renal antioxidant enzymes (SOD and catalase) after UUO. Significantly inhibited UUOinduced elevated plasma AngII and TGF-β1 levels, TGF-β1 protein expression and Smad3 phosphorylation.
KS370G is an orally active hypoglycemic and cardiovascular protective agent. KS370G improves left ventricular hypertrophy and function in pressure-overload mice heart. KS370G reduces renal obstructive nephropathy.
体内研究：
KS370G (1 mg/kg; oral; once daily for 8 weeks) 通过降低压力过载小鼠心脏 ERK、AKT 和 GSK3β 的磷酸化，改善左心室功能，抑制心脏肥厚。 KS370G (10 mg/kg; oral; once daily for 13 days) 通过减少小鼠炎症和氧化应激减轻单侧输尿管梗阻引起的肾纤维化。Animal Model:Pressure-overload ICR mice model
Dosage:1 mg/kg
Administration:Oral gavage, once daily for 8 weeks
Result:Inhibited cardiac hypertrophy and improved cardiac function induced by pressure overload. Decreased the plasma levels of atrial natriuretic peptide and lactate dehydrogenase. Significantly reduced pressure overload-induced increase of α-SMA and phosphorylation of ERK, AKT and GSK3β. Reduced cardiac collagen accumulation.
Animal Model:Male ICR mice, unilateral ureteral obstruction (UUO) model
Dosage:10 mg/kg
Administration:Oral, once daily for 13 days
Result:Significantly attenuated collagen deposition in the obstructed kidney and inhibited UUO-induced renal fibrosis markers expression, including fibronectin, type I collagen, vimentin, and α-smooth muscle actin (α-SMA). Significantly lowered the expression of renalinflammatory chemokines/adhesion molecules and monocyte cells marker (MCP-1, VCAM-1, ICAM-1 and CD11b). Reduced renal malondialdehyde levels and reversed the expression of renal antioxidant enzymes (SOD and catalase) after UUO. Significantly inhibited UUOinduced elevated plasma AngII and TGF-β1 levels, TGF-β1 protein expression and Smad3 phosphorylation.
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