脓毒症引起的心肌细胞损伤是临床常见危重症的并发症,是重症监护病房(ICU)患者高死亡率的重要原因。因此,我们利用脂多糖(LPS)诱导的H9c2细胞体外模拟心肌细胞损伤。本研究旨在探讨X-box结合蛋白1 (X-box binding protein 1, XBP1)是否通过激活NF-κB信号通路,下调Xlinked inhibitor of apoptosis protein (XIAP),从而加重lps诱导的心肌细胞损伤。转染或LPS诱导后,采用RT-qPCR和Western blot检测XBP1的表达。采用MTT法和TUNEL法检测H9c2细胞活力和凋亡。Western blot检测凋亡及NF-κB信号通路相关蛋白表达。用他们的商用试剂盒评估H9c2细胞的炎症和氧化应激。采用双荧光素酶报告基因法和染色质免疫沉淀(CHIP)法检测XBP1和XIAP的联合用药。因此,LPS促进了H9c2细胞中XBP1的表达。XBP1联合XIAP。 Inhibition of XBP1 increased viability, and inhibited apoptosis, inflammation, and oxidative stress of LPS-induced H9c2 cells by suppressing the NF-κB signaling pathway, which was partially reversed by the inhibition of XIAP. In conclusion, inhibition of XBP1 alleviates LPS-induced cardiomyocytes injury by upregulating XIAP through suppressing the NF-κB signaling pathway.

参考文献

PubMed