In Vivo |
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[1]。 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[2]。 Animal Model: Pressure-overload ICR mice model[1] 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[2] 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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