...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Shock: Molecular, cellular, and systemic pathobiological aspects and therapeutic approaches = The official journal of the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies >Diverse cardioprotective signaling mechanisms of peroxisome proliferator-activated receptor-gamma ligands, 15-deoxy-Delta12,14-prostaglandin J2 and ciglitazone, in reperfusion injury: role of nuclear factor-kappaB, heat shock factor 1, and Akt.
【24h】

Diverse cardioprotective signaling mechanisms of peroxisome proliferator-activated receptor-gamma ligands, 15-deoxy-Delta12,14-prostaglandin J2 and ciglitazone, in reperfusion injury: role of nuclear factor-kappaB, heat shock factor 1, and Akt.

机译：不同的心血管信号机制过氧物酶体proliferator-activated receptor-gamma配体、15-deoxy-Delta12 14-prostaglandin J2和ciglitazone,在再灌注损伤作用核factor-kappaB,热休克因子1,

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a nuclear receptor that regulates diverse biological functions including inflammation. The PPARgamma ligands have been reported to exert cardioprotective effects and attenuate myocardial reperfusion injury. Here, we examined the molecular mechanisms of their anti-inflammatory effects. Male Wistar rats were subjected to myocardial ischemia and reperfusion and were treated with the PPAR-gamma ligands, 15-deoxy-Delta-prostaglandin J2 (15d-PGJ2) or ciglitazone, or with vehicle only, in the absence or presence of the selective PPAR-gamma antagonist GW-9662. In vehicle-treated rats, myocardial injury was associated with elevated tissue activity of myeloperoxidase, indicating infiltration of neutrophils, and elevated plasma levels of creatine kinase and tumor necrosis factor-alpha. These events were preceded by activation of the nuclear factor-kappaB pathway. The PPAR-gamma DNA binding was also increased in the heart after reperfusion. Treatmentwith ciglitazone or 15d-PGJ2 reduced myocardial damage and neutrophil infiltration and blunted creatine kinase levels and cytokine production. The beneficial effects of both ligands were associated with enhancement of PPAR-gamma DNA binding and reduction of nuclear factor-kappaB activation. Treatment with 15d-PGJ2, but not ciglitazone, enhanced DNA binding of heat shock factor 1 and upregulated the expression of the cardioprotective heat shock protein 70. Treatment with 15d-PGJ2, but not ciglitazone, also induced a significant increase in nuclear phosphorylation of the prosurvival kinase Akt. The cardioprotection afforded by ciglitazone was attenuated by the PPAR-gamma antagonist GW-9662. In contrast, GW-9662 did not affect the beneficial effects afforded by 15d-PGJ2. Thus, our data suggest that treatment with these chemically unrelated PPAR-gamma ligands results in diverse anti-inflammatory mechanisms.
机译：过氧物酶体proliferator-activated receptor-gamma()γ- ppar是核受体调节不同生物功能包括炎症。据报道,发挥心血管效应减弱心肌再灌注损伤。检查他们的分子机制抗炎效果。心肌缺血和再灌注与配体,γ- ppar治疗15-deoxy-Delta-prostaglandin J2 (15 d-pgj2)或ciglitazone或车辆,没有或选择性- ppar的存在拮抗剂gw - 9662。心肌损伤与升高有关组织髓过氧化物酶活性,表明中性粒细胞的浸润,提高等离子体肌酸激酶水平和肿瘤坏死因子-α。核factor-kappaB通路的激活。DNA结合γ- ppar也在增加再灌注后心脏。ciglitazone或15 d-pgj2减少心肌损伤和中性粒细胞浸润,肌酸被削弱激酶水平和细胞因子的生产。有利影响的配体与DNAγ- ppar的增强有关绑定和减少核factor-kappaB激活。ciglitazone、增强的DNA结合热休克因子1和调节的表达护心热休克蛋白70。但不是ciglitazone 15 d-pgj2也诱导核磷酸化的显著增加prosurvival激酶的一种蛋白激酶。心脏保护提供ciglitazone减毒的拮抗剂γ- ppar gw - 9662。相比之下,gw - 9662没有影响15 d-pgj2提供有益的影响。我们的数据表明,这些治疗化学配体γ- ppar无关的结果在不同的抗炎机制。

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号