包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
5mg | 电议 |
10mg | 电议 |
50mg | 电议 |
100mg | 电议 |
Cell lines | human umbilical mesenchymal stem cells(HUMSCs) |
Preparation Method | MTT assay was used to test the toxicity of VX-765. Oxygen-glucose deprivation (OGD) was applied to mimic ischemic environment in vitro experiments, and The apoptosis of HUMSCs incubated with VX-765 was assessed 12 or 24 hours after OGD exposure. |
Reaction Conditions | 10μM VX-765 for 12, 24h. |
Applications | Compared to OGD groups, TUNEL-positive cells, IL-1β, and IL-6 decreased while IL-10 increased in VX-765+OGD group. The result demonstrate the anti-apoptosis and anti- inflammatory role of VX-765 in HUMSCs. |
Animal models | CD1 (ICR) mice |
Preparation Method | CD1 (ICR) mice were injected intraperitoneally with 55 mg/kg streptozotocin(STZ). Mice with blood glucose level over 300 mg/dL were considered diabetic.Diabetic mice were administered with VX-765 for 8 weeks.The treatment with VX-765 was initiated 2 weeks after STZ injection |
Dosage form | 100mg/kg VX-765, intraperitoneal(i.p.) injection |
Applications | Administration of VX-765 in diabetic mice effectively ameliorated renal function, compared with that of untreated diabetic mice.VX-765 treatment did not affect blood glucose level or body weight, illustrating that VX-765 ameliorated diabetic nephropathy independent of its metabolic effects. |
文献引用 | |
产品描述 | VX-765 is a newly developed, selective, small molecule caspase-1 inhibitor that can pass the blood-brain barrier and reduce inflammation in vitro and in vivo[1]. VX-765 potently and specifically inhibited human Casp1 (IC50 3.68 nM)[2]. Increases of autophagy-related proteins were detected in VX-765-pretreated human umbilical mesenchymal stem cells(HUMSCs), indicating the potential of VX-765 for up-regulating autophagy. Meanwhile, increased p-AMPK and decreased p-mTOR were detected in VX-765-pretreated HUMSCs. Furthermore, the anti-inflammatory and anti-apoptosis effect of VX-765 could be abolished by an autophagy inhibitor or AMPK inhibitor[3] In vivo,VX-765 ameliorated renal dysfunction, tubular injury, and renal inflammation in mice with DN, but had no effect on blood glucose level or body weight, illustrating that VX-765 represents a novel and efficacious therapeutic treatment for DN without increasing the risk of hypoglycemia in diabetic patients[4] References: |