特丁基对苯二酚作用机制 - Medchemexpress - MCE中国

1、Product Data SheetTBHQCat. No.: HY-100489CAS No.: 1948-33-0分式: CHO分量: 166.22作靶点: Keap1-Nrf2; ERK; Autophagy; Apoptosis; Ferroptosis作通路: NF-B; MAPK/ERK Pathway; Stem Cell/Wnt; Autophagy; Apoptosis储存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性数据体外实验 DMSO : 56.66 mg/mL (340.8

2、7 mM)* means soluble, but saturation unknown.SolventMass1 mg 5 mg 10 mgConcentration制备储备液1 mM 6.0161 mL 30.0806 mL 60.1612 mL5 mM 1.2032 mL 6.0161 mL 12.0322 mL10 mM 0.6016 mL 3.0081 mL 6.0161 mL请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存式和期限：-80C, 6 months; -20C, 1 month。-80C 储存时，请

3、在 6 个内使，-20C 储存时，请在 1 个内使。体内实验请根据您的实验动物和给药式选择适当的溶解案。以下溶解案都请先按照 In Vitro 式配制澄清的储备液，再依次添加助溶剂：为保证实验结果的可靠性，澄 的储备液可以根据储存条件，适当保存；体内实验的作液，建议您现现配，当天使； 以下溶剂前显的百分 指该溶剂在您配制终溶液中的体积占；如在配制过程中出现沉淀、析出现象，可以通过加热和/或超声的式助溶1. 请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (15.04 mM); Clear so

4、lution此案可获得 2.5 mg/mL (15.04 mM，饱和度未知) 的澄清溶液。以 1 mL 作液为例，取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 400 L PEG300 中，混合均匀；向上述体系中加50 L Tween-80，混合均匀；然后继续加 450 L 理盐定容 1 mL。2. 请依序添加每种溶剂： 10% DMSO 90% (20% SBE-CD in saline)Solubility: 2.5 mg/mL (15.04 mM); Clear solutionPage 1 of 2 www.MedChemE此案可获得 2.5 mg/mL (15.0

5、4 mM，饱和度未知) 的澄清溶液。以 1 mL 作液为例，取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 900 L 20% 的 SBE-CD 理盐溶液中，混合均匀。3. 请依序添加每种溶剂： 10% DMSO 90% corn oilSolubility: 2.5 mg/mL (15.04 mM); Clear solution此案可获得 2.5 mg/mL (15.04 mM，饱和度未知) 的澄 溶液，此案不适于实验周 期在半个以上的实验。以 1 mL 作液为例，取 100 L 25.0 mg/mL 的澄 DMSO 储备液加到 900 L 油中，混合均匀。BIOLOGI

6、CAL ACTIVITY物活性 TBHQ (tert-Butylhydroquinone)种泛使的 Nrf2 激活剂，通过激活 Nrf2 来免受 Doxorubicin (DOX)-诱导的脏毒性1。TBHQ (tert-Butylhydroquinone) 也 种 ERK 激活剂，逆转 Dehydrocorydaline (DHC) 对素瘤细胞增殖的抑制作2。IC & Target ERK Nrf2 Autophagy体外研究TBHQ (t-butylhydroquinone; tBHQ; 0-100 M; 48 hours; H9c2 cells) alone does not affect

7、 H9c2 cells viability. Pre-incubation of the H9c2 cells with various concentrations of tBHQ for 24 hours enhances cell viability which isdecreased due to exposure to ethanol in a dose-dependent manner. Treatment with tBHQ markedly enhances theviability of H9c2 cardiomyocytes exposed to ethanol3.TBHQ

8、 (5 M; 15 min; H9c2 cells) treatment significantly reduces the amount of apoptotic cells exposed to ethanol3.TBHQ (5 M; H9c2 cells) pre-treatment markedly inhibites the ethanol-induced increase in caspase-3 and Baxexpression, and enhances Bcl-2 expression3.Cell Viability Assay3Cell Line: H9c2 cellsC

9、oncentration: 0 M, 0.625 M, 1.25 M, 2.5 M, 5 M, 10 M, 20 M, 50 M and 100 MIncubation Time: 48 hoursResult: Enhanced the viability of H9c2 cardiomyocytes exposed to ethanol.Apoptosis Analysis3Cell Line: H9c2 cellsConcentration: 5 MIncubation Time:Result: Lowered the amount of apoptotic cells exposed

10、to ethanol.Western Blot Analysis3Cell Line: H9c2 cellsConcentration: 5 MIncubation Time:Result: Inhibited the ethanol-induced increase in caspase-3 and Bax expression, andPage 2 of 3 www.MedChemEenhanced Bcl-2 expression.体内研究 TBHQ treatment (50 mg/kg; Intraperitoneal injection; three injections at i

11、ntervals of 8 h that began 1-h post ICH; CD-1mice) augments the DNA-Binding activity of Nrf2, attenuates oxidative brain damage and acute neurological deficitsafterintracerebral hemorrhage (ICH), attenuates microglial activation with concomitant reduction in the release ofproinflammatory cytokine in

12、terleukin-1 (IL-1). TBHQ has the efficacy of post-injury administration in attenuatingacute neurological injury after ICH4.Animal Model: Male CD-1 mice (8-10 weeks old)4Dosage: 50 mg/kgAdministration: Intraperitoneal injection; three injections at intervals of 8 hours that began 1h postICH.Result: T

13、he treatment augmented the DNA-binding activity of Nrf2, attenuated brainoxidative damage, attenuated the microglial activation and the expression of IL-1.户使本产品发表的科研献 Proc Natl Acad Sci U S A. 2019 Feb 19;116(8):2996-3005. J Neuroinflammation. 2019 Oct 4;16(1):185. Oxid Med Cell Longev. 2020 May. Bi

14、ochem Pharmacol. 2019 Oct 17:113673. Front Pharmacol. 2018 Jun 6;9:540.See more customer validations on HYPERLINK www.MedChemE www.MedChemEREFERENCES1. Lin-Feng Wang, et al. Tert-butylhydroquinone ameliorates doxorubicin-induced cardiotoxicity by activating Nrf2 and inducing the expression of itstar

15、get genes. Am J Transl Res. 2015; 7(10): 17241735.2. Hu H, et al. Dehydrocorydaline inhibits cell proliferation, migration and invasion via suppressing MEK1/2-ERK1/2 cascade in melanoma.Onco TargetsTher. 2019 Jul 2;12:5163-5175.3. XIAOJING SHI, et al. Tert-butylhydroquinone attenuates the ethanol-in

16、duced apoptosis of and activates the Nrf2 antioxidant defense pathway in H9c2cardiomyocytes.Int J Mol Med. 2016 Jul; 38(1): 123130.4. Sukumari-Ramesh S, et al. Post-Injury Administration of Tert-butylhydroquinone Attenuates Acute Neurological Injury AfterIntracerebral Hemorrhage inMice.J Mol Neurosci. 201