Application
一种选择性的SIRT3抑制剂，IC50:16 nM。有比对SIRT1和SIRT2更强的选择性，对其IC50值为88 nM 和 92 nM。
In Vitro：3-TYP inhibits melatonin-enhanced SIRT3 activity but does not affect SIRT3 protein expression. 3-TYP pretreatment reverses the protective effects of melatonin on cadmium (Cd)-induced mitochondrial-derived O2?? production and autophagic cell death. 3-TYP significantly attenuates melatonin-induced increases in deacetylated-SOD2 expression and SOD2 activity in HepG2 cells exposed to Cd.
In Vivo：3-TYP (50 mg/kg, i.p.) does not significantly influence the LVEF, LVFS, infarct size, serum LDH levels, apoptosis, and oxidative stress compared with those of the Sham group. Moreover, 3-TYP has little effect on gp91phox, Nrf2, NQO 1, Bax, Bcl-2, Caspase-3, and cleaved Caspase-3 expression levels, compared with the Sham group. 3-TYP significantly decreases SIRT3 activity and increases the acetylation of SOD2 compared with that in the control group, without influencing SIRT3 expression. 3-TYP attenuates the cardioprotective effects of melatonin by decreasing the LVEF and LVFS after 24 hour of reperfusion. 3-TYP also increases the infarct size, serum LDH levels, and apoptotic ratio compared with those in the IR+Mel group.
体外：3-TYP抑制褪黑激素增强的SIRT3活性，但不影响SIRT3蛋白表达。 3-TYP预处理可逆转褪黑素对镉（Cd）诱导的线粒体来源的O2的保护作用。产生和自噬细胞死亡。 3-TYP显着减弱褪黑素诱导的Cd暴露的HepG2细胞中脱乙酰化SOD2表达和SOD2活性的增加。
体内：与假手术组相比，3-TYP（50 mg / kg，腹膜内）对LVEF，LVFS，梗死面积，血清LDH水平，细胞凋亡和氧化应激没有显着影响。此外，与Sham组相比，3-TYP对gp91phox，Nrf2，NQO 1，Bax，Bcl-2，Caspase-3和裂解的Caspase-3表达水平几乎没有影响。与对照组相比，3-TYP显着降低SIRT3活性并增加SOD2的乙酰化，而不会影响SIRT3的表达。 3-TYP在再灌注24小时后通过降低LVEF和LVFS来减弱褪黑激素的心脏保护作用。与IR + Mel组相比，3-TYP还增加了梗塞面积，血清LDH水平和细胞凋亡率。
性质
| Iupac Name： | 3-(1H-1,2,3-triazol-4-yl)pyridine |
| Inchi Code | 1S/C7H6N4/c1-2-6(4-8-3-1)7-5-9-11-10-7/h1-5H,(H,9,10,11) |
| Inchi Key | VYXFEFOIYPNBFK-UHFFFAOYSA-N |
安全信息
RIDADR NONH for all modes of transport
