茴香霉素作用機(jī)制 - Medchemexpress - MCE中國

1、Product Data SheetAnisomycinCat. No.: HY-18982CAS No.: 22862-76-6分式: CHNO分量: 265.31作靶點(diǎn): DNA/RNA Synthesis; JNK; Bacterial; Apoptosis作通路: Cell Cycle/DNA Damage; MAPK/ERK Pathway; Anti-infection; Apoptosis儲(chǔ)存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-20C 1 month溶解性數(shù)據(jù)體外實(shí)驗(yàn) DMSO : 50 mg/mL (

2、188.46 mM)* means soluble, but saturation unknown.SolventMass1 mg 5 mg 10 mgConcentration制備儲(chǔ)備液1 mM 3.7692 mL 18.8459 mL 37.6918 mL5 mM 0.7538 mL 3.7692 mL 7.5384 mL10 mM 0.3769 mL 1.8846 mL 3.7692 mL請根據(jù)產(chǎn)品在不同溶劑中的溶解度選擇合適的溶劑配制儲(chǔ)備液；旦配成溶液，請分裝保存，避免反復(fù)凍融造成的產(chǎn)品失效。儲(chǔ)備液的保存式和期限：-80C, 6 months; -20C, 1 month。-80C 儲(chǔ)

3、存時(shí)，請?jiān)?6 個(gè)內(nèi)使，-20C 儲(chǔ)存時(shí)，請?jiān)?1 個(gè)內(nèi)使。體內(nèi)實(shí)驗(yàn)請根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥式選擇適當(dāng)?shù)娜芙獍?。以下溶解案都請先按?In Vitro 式配制澄清的儲(chǔ)備液，再依次添加助溶劑：為保證實(shí)驗(yàn)結(jié)果的可靠性，澄 的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；體內(nèi)實(shí)驗(yàn)的作液，建議您現(xiàn)現(xiàn)配，當(dāng)天使； 以下溶劑前顯的百分 指該溶劑在您配制終溶液中的體積占；如在配制過程中出現(xiàn)沉淀、析出現(xiàn)象，可以通過加熱和/或超聲的式助溶1. 請依序添加每種溶劑： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (9.42 mM); Clear

4、 solution此案可獲得 2.5 mg/mL (9.42 mM，飽和度未知) 的澄清溶液。以 1 mL 作液為例，取 100 L 25.0 mg/mL 的澄 DMSO 儲(chǔ)備液加到 400 L PEG300 中，混合均勻；向上述體系中加50 L Tween-80，混合均勻；然后繼續(xù)加 450 L 理鹽定容 1 mL。2. 請依序添加每種溶劑： 10% DMSO 90% (20% SBE-CD in saline)Solubility: 2.5 mg/mL (9.42 mM); Clear solutionPage 1 of 2 www.MedChemE此案可獲得 2.5 mg/mL (9.4

5、2 mM，飽和度未知) 的澄清溶液。以 1 mL 作液為例，取 100 L 25.0 mg/mL 的澄 DMSO 儲(chǔ)備液加到 900 L 20% 的 SBE-CD 理鹽溶液中，混合均勻。3. 請依序添加每種溶劑： 10% DMSO 90% corn oilSolubility: 2.5 mg/mL (9.42 mM); Clear solution此案可獲得 2.5 mg/mL (9.42 mM，飽和度未知) 的澄 溶液，此案不適于實(shí)驗(yàn)周 期在半個(gè)以上的實(shí)驗(yàn)。以 1 mL 作液為例，取 100 L 25.0 mg/mL 的澄 DMSO 儲(chǔ)備液加到 900 L 油中，混合均勻。BIOLOGICA

6、L ACTIVITY物活性 Anisomycin種有效的蛋質(zhì)合成抑制劑，它通過抑制肽 轉(zhuǎn)移酶80核糖體系統(tǒng)擾蛋質(zhì)和 DNA 合成。Anisomycin 種 JNK 激活劑，可增強(qiáng)磷酸化 JNK 。Anisomycin 從灰鏈霉 中分離出的種細(xì) 抗素。IC & Target JNK DNA synthesis體外研究 To examine whether JNK has a core role in colistin-induced neurotoxicity in PC-12 cells, an SP600125 (a highlyselective inhibitor of JNK) and

7、 Anisomycin (a potent activator) are used in this study. In order to select an appropriateconcentration, PC-12 cells are treated with a range of SP600125 (0-80 M) and Anisomycin (0-20 M) respectively for24 h. The results show that the cells viability significantly decreases by SP600125 treatment in

8、a concentration-dependent manner, observed at the concentrations greater than 20 M (p0.01). Similarly the cells viability isinhibited by Anisomycin treatment (8 M) (p0.05) 1.體內(nèi)研究 Disruption of TNFRp55/p75 attenuates Anisomycin-induced ventricular functional improvements. Anisomycin resultsin an impr

9、ovement in left ventricular developed pressure (LVDP), which disappears in animals with disruption of TNFR p55/p75. In addition, the Anisomycin-induced improvement in LVEDP in wild-type animals is eliminated by deletionof TNFR p55/p75. Likewise, disruption of TNFR p55/p75 abrogates the recovery of r

10、ate pressure product (RPP) elicitedby pretreatment of Anisomycin. TNFR p55/p75-/- mice without Anisomycin treatment do not show differences incardiac functional recovery compared with the control wild-type mice. There are no significant differences in heartrate between wild-type and TNFR p55/p75-def

11、icient mice. To see whether Nox2 is involved in Anisomycin-inducedmyocardial protection, Nox2-deficient mice are treated with Anisomycin. The improvement in the LVEDP inAnisomycin-treated mice is eliminated in Nox2-/- mice compared with wild-type mice. In addition, recovery of RPP inwild-type mice t

12、reated with Anisomycin is mitigated in Nox2-/- mice. Nox2-/- mice without Anisomycin treatment donot show the difference in cardiac functional recovery compared with wild-type control mice2.PROTOCOLCell Assay 1 PC-12 cells are seeded in 96-well plates at a concentration of 1104 cells/well and cultur

13、ed in an incubator at 37Cwith 5% CO2 for at least 12 h prior to exposure to different concentrations of SP600125 (0-80 M) or Anisomycin (0-20 M) for 24 h. Subsequently, the culture medium is added to 20 L of 5 mg/mL MTT working solution and theplate is incubated for 2 h at 37C. The culture supernata

14、nt is removed and the formazan crystals are dissolved in 150L DMSO. Finally, the absorbance of each well is measured at 490 nm by a microplate reader. Cell viability isexpressed as the percentage of the control group, which is set to 100%1.MCE has not independently confirmed the accuracy of these me

15、thods. They are for reference only.Animal Mice2Administration 2 Adult male TNFRp55/p75 mice, adult male wild-type C57/BL and homozygous Nox2-/- mice are used in this study.Mice are randomized into six experimental groups that undergo the following treatments,. Animals are divided intoPage 2 of 3 www

16、.MedChemEsix groups: group 1: control ischemia/reperfusion, wild-type mice are injected with DMSO (0.1 mL); group 2:Anisomycin+wild-type mice, wild-type mice are injected with Anisomycin (0.1 mg/kg ip); group 3: Anisomycin+TNFRp55/p75-/- mice, TNFR p55/75-/- mice are injected with Anisomycin (0.1 mg

17、/kg ip); group 4: TNFR p55/p75-/- mice,TNFR p55/75-/- mice are not injected with Anisomycin; group 5: Anisomycin+Nox2-/- mice, Nox2-/- mice are injectedwith Anisomycin (0.1 mg/kg ip); and group 6: Nox2-/- mice, Nox2-/- mice are not injected with Anisomycin. Later (24h), the hearts are subjected to 3

18、0 min of ischemia followed by 30 min of reperfusion2.MCE has not independently confirmed the accuracy of these methods. They are for reference only.戶使本產(chǎn)品發(fā)表的科研獻(xiàn) J Hazard Mater. 2020 May. J Exp Clin Cancer Res. 2020 Feb 5;39(1):29. Am J Physiol Cell Physiol. 2018 Aug 1;315(2):C225-C235. Sci Rep. 2018

19、Apr 23;8(1):6379. Sci Rep. 2017 Oct 19;7(1):13571.See more customer validations on HYPERLINK www.MedChemE www.MedChemEREFERENCES1. Lu Z, et al. Colistin-induced autophagy and apoptosis involves the JNK-Bcl2-Bax signaling pathway and JNK-p53-ROS positive feedback loop in PC-12cells.2. Zhao TC, et al. Disruption of Nox2 and TNFRp55/p75 eliminates cardioprotection in