| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 50mg | 电议 |
Preparation Method | Purified protein containing PDE3, 4 or 5 enzyme was resuspended in 50 mM Tris HCl containing 5 mM MgCl2 (pH 7.5). Subsequently, the enzyme (11.5 mg ml 1, 10 μl) was incubated with Tris HCl (80 μl) and 10 μM cyclic GMP or cyclic AMP substrate (final concentration 1 μM containing 0.1 μCi [3H]-cyclic GMP or [3H]-cyclic AMP) was added. After 20 min at 37 ℃, the samples were heated to 100 ℃ for 2 min. Ophiophagus hannah snake venom (10 mg ml 1, 10 μl) was then added and incubated at 37 ℃ for 10 min to convert the 5 -GMP and 5 -AMP to the uncharged nucleosides, guanosine and adenosine, respectively. An ion-exchange resin (200 μl) was added to bind all unconverted cyclic GMP or cyclic AMP. IBMX as inhibitor, used to inhibit PDE detection IC50. |
Reaction Conditions | IBMX 10 mM in DMSO |
Applications | IBMX is a broad-spectrum phosphodiesterase (PDE) inhibitor that inhibits PDE3,PDE4 and PDE5 with IC50 values of 6.5,26.3 and 31.7 μm, respectively. |
Cell lines | Cortical collecting duct (CCD) |
Preparation Method | Cells were grown in 24-well plates with 105 cells per well at confluence, monolayers were washed with phosphate buffer solution (PBS) and incubated with KMUP-1 (0.1-100μM) in the presence of 100uM IBMX for 20 min by adding 10% trichloroacetic acid (TCA) to stop the incubation. |
Reaction Conditions | 100μM IBMX for 20 minutes |
Applications | IBMX (100 μM) activates renal outer medullary K+ (ROMK) channels (n=6, P<0.05) and prevents further channel activation by ANG II (n=6, P=NS) or cGMP. Of note is that pretreatment of cortical collecting duct (CCDs) isolated from high-K+ (HK)-fed rats with IBMX (100 μM) for 20 min leads to a significant increase in tubular cAMP content to 1.43±0.35 pg/mm tubule length (n=14) compare with that measured in vehicle-treated controls. |
Animal models | Six groups of male Sprague–Dawley rats were used (150?80 g) |
Preparation Method | After 8 weeks of exposure to cold, 3 groups in each temperature condition received continuous intravenous infusion of 8-isobutyl-methylxanthine (8-IBMX) (PDE-1 inhibitor, 8.5 mg/kg per day),apocynin and vehicle. |
Dosage form | 8.5 mg/kg/day for 1 week |
Applications | Treatments with IBMX and Apocynin significantly decrease cold-induced elevation of right ventricular (RV) systolic pressure although they do not decrease RV pressure to the warm control levels. IBMX or Apocynin significantly reduces medial layer thickness and increases lumen diameter of small PAs in cold-exposed rats. |
| 产品描述 | IBMX is a non-specific inhibitor of phosphodiesterase (PDE) inhibitor that inhibits PDE3, PDE4 and PDE5 with IC50 values of 6.5, 26.3 and 31.7 µm, except PDE8A, PDE8B and PDE9[1,7]. In cardiac H9c2 cells,IBMX reduced loss of δψm caused by H(2)O(2), indicating that inhibition of PDEs can prevent the mPTP opening. However, IBMX could not inhibit the pore opening in cells transfected with the constitutively active GSK-3β (GSK-3β-S9A) mutant, suggesting a critical role of GSK-3β in the action of IBMX. IBMX also reduced reperfusion injury in a GSK-3β dependent manner[5]. Increasing cAMP-signaling with Forskolin or IBMX significantly facilitated neuronal functional maturation. A continuous application of IBMX to the differentiation medium substantially increased the functional expression of voltage-gated Na(+) and K(+) channels, as well as neuronal firing frequency[6]. Chronic exposure to cold caused pulmonary arterial hypertension and increased phosphodiesterase-1C (PDE-1C) expression in pulmonary arteries (PAs) in rats. After 8-week exposure to cold, Treatment with 8-IBMX significantly attenuated the cold-induced increase in right ventricular pressure. Cold exposure also caused right-ventricular hypertrophy, whereas 8-IBMX reversed cold-induced right ventricular hypertrophy. 8-IBMX abolished cold-induced upregulation of PDE-1C in PAs[4]. In hyperglycemic rat, all test compounds decreased blood glucose and the effect of milrinone was potentiated by glybenclamide. Milrinone or IBMX did not change plasma insulin levels, but it was augmented by combination of milrinone and glybenclamide. In both species, liver glycogen storage was decreased by IBMX, mc5, mc6 or MCPIP, increased by mc2 and was not changed in the presence of mc1[3]. ANG II increased ROMK channel activity in CCDs isolated from high-K (HK)-fed but not normal K (NK)-fed rats. Pretreatment of CCDs with IBMX, a broad-spectrum PDE inhibitor, or cilostamide, a PDE3 inhibitor, abolished the stimulatory effect of ANG II on ROMK channels[2]. References: |
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