| 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 | HepG2 cells |
Preparation Method | HepG2 cells were pretreated with 3-TYP (50 μM) or the vehicle for 1 h, followed by the treatment with DHM (20 μM) for 2 h and 0.2 mM of PA for 16 h. |
Reaction Conditions | 50 μM, 16h |
Applications | DHM treatment attenuates PA-induced autophagy arrest and oxidative stress in hepatocytes, which was mediated via SIRT3. |
Animal models | C57BL/6 J male mice |
Preparation Method | Both 3-TYP and 2-methoxyestradiol were administered by intraperitoneal injection starting 1 week prior to NE for 7 days 3-TYP was administered at 50 mg/kg/day, and 2-ME was administered at 16 mg/kg/day. |
Dosage form | 50 mg/kg/day,i.p. |
Applications | 3-TYP exacerbates noise-induced hair cell damage; 3-TYP increases the acetylation level of SOD2 and aggravates oxidative stress and apoptosis. |
| 产品描述 | 3-TYP inhibit SIRT3 with an IC50 of 16 nM, and is more potent over SIRT1 and SIRT2 with IC50 of 88 nM and 92 nM, respectively.[1] In vitro, with 50 μM 3-TYP abrogated the barrier protective effect of PD in multiple organs of septic mice. In HUVECs, 3-TYP (50 μM) diminished PD-mediated protection against F-actin redistribution, cadherin–catenin complex dissociation, and endothelial monolayer hyperpermeability.[3]In vitro study it demonstrated that at 100 μM, 3-TYP decreased expression of genes involved in lipolysis and glucose transport GLUT4 compared to HNK. At the meantime, 3-TYP also caused an increase in gene expression of adipocyte-specific cytokines, including IL6, resistin, and TNF-α. In vitro, treatment with 100 μM 3-TYP obviously inhibited glucose uptake in 3T3-L1 adipocytes in contrast to control in the presence of insulin.[5]In A/R-treated H9c2 cells, 4-P-PDOT (10 μM) and 3-TYP (5 μM) treatment resulted in no notable difference in cell viability. In addition, combination wiith 4-P-PDOT and 3-TYP elevated apoptotic signaling by increasing cleaved caspase-3 and Bax expression while decreasing Bcl-2 expression compared with that in the A/R + Mel group.[6] In vivo experiment it suggested that treatment with 50 mgkg intraperitoneally 3-TYP reversed the induction of mitophagy by decreasing the expression levels of FOXO3α, BINP3, LC3-II/LC3-I, SOD2, PRDX3, and P62.[2]In vivo efficacy test it indicated that C57BL/6 mice were administrated 50 mg/kg 3-TYP abolished TBM's antioxidative effects.[4] References: |
m.cnreagent.com