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活化蛋白 C 诱导内质网应激并减弱糖原合酶激酶-3β介导的脂多糖诱导的细胞凋亡。

Activated protein C induces endoplasmic reticulum stress and attenuates lipopolysaccharide-induced apoptosis mediated by glycogen synthase kinase-3β.

机构信息

Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing 210002, China.

出版信息

Mediators Inflamm. 2012;2012:485279. doi: 10.1155/2012/485279. Epub 2012 May 28.

Abstract

This study investigated the relationship between antiapoptotic activities induced by activated protein C and endoplasmic reticulum stress. In this study, it was observed that activated protein C elicited a rise in glucose-regulated protein 78 and glycogen synthase kinase-3β and inhibited apoptosis in human umbilical vein endothelial cells induced by lipopolysaccharide. Calcium inhibition did not alter the antiapoptotic effect of activated protein C. The antiapoptotic efficiency of activated protein C was reduced in human umbilical vein endothelial cells following treatment with glycogen synthase kinase-3β-siRNA. In summary, activated protein C induced endoplasmic reticulum stress and attenuated lipopolysaccharide-induced human umbilical vein endothelial cell apoptosis mediated by glycogen synthase kinase-3β.

摘要

本研究探讨了激活蛋白 C 诱导的抗凋亡活性与内质网应激之间的关系。在这项研究中,观察到激活蛋白 C 引起葡萄糖调节蛋白 78 和糖原合酶激酶-3β 的增加,并抑制脂多糖诱导的人脐静脉内皮细胞凋亡。钙抑制不改变激活蛋白 C 的抗凋亡作用。糖原合酶激酶-3β-siRNA 处理后人脐静脉内皮细胞中激活蛋白 C 的抗凋亡效率降低。总之,激活蛋白 C 诱导内质网应激,并减弱糖原合酶激酶-3β 介导的脂多糖诱导的人脐静脉内皮细胞凋亡。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/71c0/3368528/d33cfe229e11/MI2012-485279.001.jpg

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