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3-TYP
本产品不向个人销售,仅用作科学研究,不用于任何人体实验及非科研性质的动物实验。
3-TYP图片
CAS NO:120241-79-4
规格:≥98%
包装与价格:
包装价格(元)
1mg电议
2mg电议
5mg电议
10mg电议
25mg电议
50mg电议
100mg电议
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产品介绍
理化性质和储存条件


Name: 3-TYP
CAS#: 120241-79-4
Chemical Formula: C7H6N4
Exact Mass: 146.0592
Molecular Weight: 146.153
Storage-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Technical Information

Solubility in DMSO: 20-30 mg/mL

Solubility in Water (warmed with 50oC water bath): 1~2 mg/mL

Synonym: 3-TYP; 3 TYP; 3TYP

Chemical Name: 3-(1H-1,2,3-triazol-4-yl) pyridine
InChi Key: VYXFEFOIYPNBFK-UHFFFAOYSA-N
InChi Code: InChI=1S/C7H6N4/c1-2-6(4-8-3-1)7-5-9-11-10-7/h1-5H,(H,9,10,11)
SMILES Code: C1(C2=CNN=N2)=CC=CN=C1
实验参考方法
Target

SIRT3:16 nM (IC50)

SIRT1:88 nM (IC50)

SIRT2:92 nM (IC50)

In Vitro3-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 O2o– 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[1].
In Vivo3-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[2].
Cell AssayCell viability is analyzed using Cell Counting Kit-8. Briefly, 1×104 cells are inoculated into 96-well plates. After being treated, 90 μL of medium and 10 μL of CCK-8 solution are added to each well. The cells are then incubated at 37°C for 2 h. After incubation, the absorption at 450 nm is measured using an Infinite(TM) M200 Microplate Reader. The results are expressed as a percentage of the control. The cell death is also evaluated using the trypan blue assay. HepG2 cells are plated in the 6-well plates (5×105 cells per well) and incubated for 24 h. After being treated with Cd or melatonin, the cells are detached with 300 μL trypsin-EDTA solution. The mixture of detached cells is centrifugated at 300 g for 5 min. Then, the residue is combined with 800 μL trypan blue solution and dispersed. After 3 min staining, cells are counted using an automated cell counter. The dead cells are stained with the blue color. Cell mortality (%) is expressed as percentage of the dead cell number/the total cell number.
Animal ExpIn brief, male C57BL/6 mice are anesthetized with 2% isoflurane, and myocardial ischemia is produced by temporarily exteriorizing the heart via a left thoracic incision and placing a 6-0 silk suture slipknot around the left anterior descending coronary artery. After 30 minutes of myocardial ischemia, the slipknot is released, and the myocardium is reperfused for 3 hour (for western blot analysis and oxidative stress measurement) or 24 hour (for cardiac function, apoptotic index and infarct size determination). Sham-operated mice undergo the same surgical procedures except the suture placed under the left coronary artery is not tied. Ten minutes before reperfusion, mice are randomized to receive either vehicle (1% ethanol) or melatonin (20 mg/kg) by intraperitoneal injection. C57BL/6 mice are randomly divided into the following groups: (i) Sham group: mice underwent the sham operation and are treated with vehicle (1% ethanol); (ii) Mel group: mice are treated with melatonin (20 mg/kg via intraperitoneal injection); (iii) IR+V group: mice underwent the MI/R operation and are treated with vehicle (1% ethanol); (iv) IR+Mel group: mice underwent the MI/R operation and are treated with melatonin (20 mg/kg via intraperitoneal injection 10 minutes before reperfusion); (v) IR+Mel+3-TYP group: mice are pretreated with 3-TYP (3-TYP is intraperitoneally injected at a dose of 50 mg/kg every 2 days for a total of three doses prior to the MI/R surgery), subjected to the MI/R operation, and treated with melatonin (20 mg/kg via intraperitoneal injection 10 minutes before reperfusion); and (vi) IR+3-TYP group: mice are pretreated with 3-TYP and then subjected to the MI/R operation.
References

[1]. SIRT3-SOD2-mROS-dependent autophagy in cadmium-induced hepatotoxicity and salvage by melatonin. Autophagy. 2015;11(7):1037-51.

[2]. Melatonin ameliorates myocardial ischemia reperfusion injury through SIRT3-dependent regulation of oxidative stress and apoptosis. J Pineal Res. 2017 Sep;63(2).

[3]. Identification of a sirtuin 3 inhibitor that displays selectivity over sirtuin 1 and 2. Eur J Med Chem. 2012 Sep;55:58-66.