首页> 外文期刊>Life sciences >Expression of COX-2 and hsp72 in peritoneal macrophages after an acute ochratoxin A treatment in mice.
【24h】

Expression of COX-2 and hsp72 in peritoneal macrophages after an acute ochratoxin A treatment in mice.

机译:小鼠急性曲霉毒素A处理后腹膜巨噬细胞中COX-2和hsp72的表达。

获取原文
获取原文并翻译 | 示例
           

摘要

Ochratoxin A (OTA) is a secondary fungal metabolite produced by Aspergillus and Penicillium strains that elicits a broad spectrum of toxicological effects in animals and man. A single oral OTA administration (10 mg/kg) in mice induced after 24 h oxidative damage and polymorphonuclear leukocyte (PMN) infiltration in parenchymal organs. In fact, OTA treatment increased lipid peroxidation (via malondialdehyde formation) in kidney and liver and PMN accumulation in duodenum, as shown by myeloperoxidase activity. Following in vivo OTA treatment an increase of cyclooxygenase-2 and of heat shock protein 72 expression was evidenced in peritoneal macrophage lysates by Western blot. That OTA modulates these proteins involved in the inflammatory process indicates that the mycotoxin is able to activate immune cells. This study suggests that the oxidative stress, the neutrophil accumulation in parenchymal tissues and the modulation of inflammatory parameters in peritoneal macrophages induced by OTA are involved in its toxicity, and represent early events related to several aspects of OTA mycotoxicosis.
机译:ch曲霉毒素A(OTA)是由曲霉和青霉菌株产生的次级真菌代谢产物,在动物和人类中引起广泛的毒理作用。在小鼠24小时氧化损伤和实质器官中的多形核白细胞(PMN)浸润后诱导小鼠口服OTA(10 mg / kg)。实际上,如髓过氧化物酶活性所示,OTA处理可增加肾脏和肝脏的脂质过氧化(通过丙二醛形成)和十二指肠中PMN的积累。在体内OTA处理后,通过Western印迹证实了腹膜巨噬细胞裂解物中环氧合酶-2和热休克蛋白72表达的增加。 OTA调节炎症过程中涉及的这些蛋白质,表明霉菌毒素能够激活免疫细胞。这项研究表明,氧化应激,中性粒细胞在实质组织中的蓄积以及OTA诱导的腹膜巨噬细胞中炎症参数的调节均与其毒性有关,并且代表了与OTA霉菌毒素中毒的多个方面有关的早期事件。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
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