1.C/EBP homologous protein gene silencing can downregulate tumor necrosis factor-α and interleukin-1β expression in models of ischemia/reperfusion injury.
2.C/EBP homologous protein not only promotes apoptosis, but also aggravates acute brain injury.
实验发现在缺血再灌注模型中,通过沉默C/EBP同源性蛋白基因可引起炎症因子肿瘤坏死因子α、白细胞介素1β的相应下调,故认为C/EBP同源性蛋白在脑缺血再灌注后不但起到促进凋亡的作用,还可能具有诱导炎症进一步加重急性脑损伤的潜在作用。