免疫印迹
细胞凋亡
流式细胞术
下调和上调
表型
医学
肝移植
内分泌学
细胞
生物
移植
肿瘤坏死因子α
内科学
免疫学
基因
生物化学
作者
Zhen Zhang,Keting Que,Yu You,Xiaoping Zhao,Diguang Wen,Zhihao Feng,Zuojin Liu
标识
DOI:10.2174/1389201022666210111113900
摘要
Objective: The purpose of this study was to explore the effect of TRAF1 on phenotypic changes of KCs in I/R in liver transplantation. Methods: SD rats were randomly divided into sham group and liver transplantation I/R group. KCs were extracted from rat livers in each group. KCs were transfected by lentivirus of si-TRAF1 or si-HOIP, and induced by Lipopolysaccharide (LPS). Flow cytometry was used to detect cell apoptosis. Western blot and RT-PCR were used to detect the protein and mRNA expression levels. Results: Compared with the sham group, the expression levels of TRAF1, TNF-α and IL-1β were significantly increased in the I/R group (P<0.05). In addition, compared with the control group, the expression levels of NF-κB (P65 and p-P65) and M1 phenotype (TNF-α and IL-1β) were notably increased in si-TRAF1 and si-HOIP group (all P<0.05). Furthermore, the levels of Linear Ubiquitin Complex (LUBAC) were markedly increased in LPS-induced KCs in comparison with the control group (P<0.05). Moreover, compared with the control group, the expression levels of P65, p-P65, TNF-α and IL-1β were notably decreased in the si-TRAF1 and si-HOIP group (P<0.05). The expression levels of P65, p-P65, TNF-α and IL-1β were significantly increased in si-TRAF1 and si-HOIP group when compared to the control group (P<0.05). Conclusion: TRAF1 was an important negative regulator of liver transplantation I/R by inhibiting the activation of NF-κB in KCs and preventing its M1 phenotype transformation.
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