| 包装 | 价格(元) |
| 2g | 电议 |
| 10g | 电议 |
| 50g | 电议 |
Cell lines | HUVEC cells |
Preparation Method | The NO donor SNP (100 μm), the NOS inhibitor L‐NAME (500 μm), and the cysteine thiol‐ educing agent TCEP hydrochloride hydrochloride (2 mm) were used to HUVEC cells. |
Reaction Conditions | 2 mm; 2h |
Applications | TCEP hydrochloride successfully abolished NO‐induced inhibition of SOD1 monomerization in HUVECs, indicating that NO inhibited monomeric SOD1 by acting on cysteine thiol |
Animal models | adult Kunming mice |
Preparation Method | Total 30 adult Kunming mice were randomly divided into normal control group (0 mg/kg·d), low-dose TCEP hydrochloride group (10 mg/kg·d), and high-dose TCEP hydrochloride group (100 mg/kg·d), and administered continuously by gavage for 30 days. |
Dosage form | 0, 10, 100 mg/kg·d; p.o. |
Applications | Compared with the control group, the water intake of high-dose TCEP hydrochloride group was declined significantly, and the organ index of liver and spleen were increased significantly. In addition, the escape latency of TCEP hydrochloride exposed mice were longer than that in the control group in water maze test, while the total swimming course of high-dose TCEP hydrochloride group was elevated and the swimming time in target quadrant was obviously shortened compared with the control group. |
| 产品描述 | TCEP hydrochloride is a non-thiol reducing agent which does not bind Hg(2+).[1]TCEP hydrochloride increased SOD1 monomer formation, thus preventing the NO‐induced increase in dismutase activity and the decrease in ROS.[5] In vitro efficacy test it shown that TCEP hydrochloride promoted NF-kappaB-DNA binding in a dose-related manner in concentrations from 0.25 to 6mM. with 6mM TCEP hydrochloride , Hg(2+) prevented NF-kappaB-DNA binding at concentrations as low as 20 microM in binding reactions.[1] In vitro experiment it indicated that treatment with 100 μM TCEP hydrochloride-HCL can improve the quality and developmental capacity of in vitro-fertilized embryos by decreasing oxidative stress in porcine oocytes.[2]In human neuronal cell line, SHSY-5Y, with 1 mM TCEP hydrochloride maximally protected against BoNT/B inhibition of [(3)H]-NA release, and has no toxic.[3]TCEP hydrochloride (0.01 mM) does not scavenge Fe(3+) from Tf and is able to protect thiol groups for the coupling to maleimide. In addition, TCEP hydrochloride does not interfere with the maleimide coupling itself.[4]In vitro, human hepatocellular (HepG2) cells were treated with 100, 200, and 400 μM TCEP hydrochloride for 3 days, the level of oxidative stress, esterase, Ca2+ influx, and ΔΨm dysfunction increased. And there were 65.96% subG1 apoptotic peak in 400 μM treated cells.[6] In vivo, treatment with 20 mg/kg and 60 mg/kg TCEP hydrochloride orally in adult ICR mice for 9 weeks, TCEP improved body weight gain, hypertriglyceridemia, and hepatic steatosis, consistent with upregulation of hepatic lipogenesis-related gene expression. TCEP also altered the levels of several hepatic metabolites.[7] References: |
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