包装 | 价格(元) |
10mM (in 1mL DMSO) | 电议 |
10mg | 电议 |
50mg | 电议 |
500mg | 电议 |
1g | 电议 |
Cell experiment: | PC-12 cells are seeded in 96-well plates at a concentration of 1×104 cells/well and cultured in an incubator at 37℃ with 5% CO2 for at least 12 h prior to exposure to different concentrations of SP600125 (0-80 μM) or Anisomycin (0-20 μM) for 24 h. Subsequently, the culture medium is added to 20 μL of 5 mg/mL MTT working solution and the plate is incubated for 2 h at 37℃. The culture supernatant is removed and the formazan crystals are dissolved in 150 μL DMSO. Finally, the absorbance of each well is measured at 490 nm by a microplate reader. Cell viability is expressed as the percentage of the control group, which is set to 100%[1]. |
Animal experiment: | Mice[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 into six 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+TNFR p55/p75-/- mice, TNFR p55/75-/- mice are injected with Anisomycin (0.1 mg/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 injected with Anisomycin (0.1 mg/kg ip); and group 6: Nox2-/- mice, Nox2-/- mice are not injected with Anisomycin. Later (24 h), the hearts are subjected to 30 min of ischemia followed by 30 min of reperfusion[2]. |
文献引用 | |
产品描述 | Anisomycin is a specific agonist of JNK with a concentration of 25 ng/ml [1]. JNK is short for c-Jun N-terminal kinase which reported as a proapoptotic kinase and plays an important role in many cellular events, such as cell cycle, proliferation, apoptosis and cell stress. It is also reported that JNK plays a pivotal role in the cell apoptosis induced by UV and activated JNK pathway could enhance TNF-α mediated apoptosis thus often regarded as a potent target in clinic [2] [3]. Anisomycin is a potent JNK agonist. When tested with hormone refractory cell line DU 145(highly resist to Fas mediated apoptosis), 250 ng/ml anisomysin treatment induced DU145 cells apoptosis together with Fas (200 ng/ml) via activating JNK [4]. In HL-60 cells, treatment of anisomysin activated JNK pathway activity which further induced cell apoptosis [5]. When tested with primary murine embryonic fibroblasts, anisomycin treatment stimulated cell apoptosis via activating JNK expression [6]. References: |