| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | HIT-T15(a pancreatic beta cell line) |
Preparation method | The solubility of this compound in DMSO is >14.3mg/mL. General tips for obtaining a higher concentration: Please warm the tube at 37℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below -20℃ for several months. |
Reacting condition | 0.5 or 1 μmol/l for 5 days |
Applications | AGEs (Advanced Glycation End-Products)-induced beta cell necrosis was completely abrogated by adding Pioglitazone to the AGEs culture medium. Pioglitazone was able to counteract AGE-induced pancreatic beta cell death and dysfunction (Adding 1 μmol/l, but not 0.5 of Pioglitazone). Taken together, pioglitazone improved insulin secretory capacity, preserving beta cell mass and islet structure and protecting beta cells from oxidative stress, as well as, improving beta cell function. |
Animal models | Eight-week-old male C57/Bl6 mice |
Dosage form | 20 mg/kg per day |
Application | Mice treated with pioglitazone were partially protected from MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine )-induced decrease of striatal dopamine concentrations at 7 days and a lower activation of microglia and less GFAP(glial fibrillary acidic protein )-positive cells in both striatum and SNpc after two and five injections of MPTP. Thus, treatment with pioglitazone completely protected TH-positive cells from MPTP toxicity in this chronic model of PD (Parkinson’s disease). In mice treated with pioglitazone, there were a reduced activation of microglia, reduced induction of NOS (NO synthase)-positive cells and less glial fibrillary acidic protein positive cells in both striatum and substantia nigra pars compacta. In addition, treatment with pioglitazone almost completely blocked staining of TH-positive neurons for nitrotyrosine, a marker of NO (nitric oxide)-mediated cell damage. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 产品描述 | Pioglitazone (U 72107) is a potent and selective PPARγ agonist with high affinity binding to the PPARγ ligand-binding domain with EC50 of 0.93 and 0.99 μM for human and mouse PPARγ, respectively. AGEs-induced beta cell necrosis is completely abrogated by adding Pioglitazone (U 72107) to the AGEs culture medium. Furthermore Pioglitazone completely prevented any AGEs-induced increment in caspase-3 activation, thereby restoring caspase-3 activity to the same levels as the control cells. As expected AG is able to counteract AGEs-induced impaired viability[2]. The serum-free fatty acid and triglyceride levels as well as adipocyte sizes in ob/ob and adipo-/- ob/ob mice are unchanged after 10 mg/kg Pioglitazone (U 72107) but are significantly reduced to a similar degree after 30 mg/kg Pioglitazone. Moreover, the expressions of TNFα and resistin in adipose tissues of ob/ob and adipo-/- ob/ob mice are unchanged after 10 mg/kg Pioglitazone but are decreased after 30 mg/kg Pioglitazone. Thus, Pioglitazone-induced amelioration of insulin resistance and diabetes may occur adiponectin dependently in the liver and adiponectin independently in skeletal muscle[3].Pioglitazone (10 mg/kg per d) treatment significantly attenuates the loss of body weight (BW) and cardiac hypertrophy. Pioglitazone treatment significantly reduces the elevated serum glucose levels and markedly improved the associated dyslipidemia. Furthermore, there is a slight but significant increase in serum creatinine level in D rats over their N controls (P<0.05). However, a marked renal dysfunction is observed in diabetic nephropathic (DN) group (P<0.05). Moreover, DN rats exhibits the highest serum activity of CK-MB, relative to both N and D rats (P<0.05). Pioglitazone is able to decrease the elevated serum levels of both creatinine and creatine kinase-MB (CK-MB)[4]. References: |
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