Inhibition of TRAF1 protects renal tubular epithelial cells against hypoxia/reoxygenation injury

Background and objective: This study aimed to explore the expression of TRAF1 in vitro kidney injury model, and the function mechanism of TRAF1 in the model growth and apoptosis.

Methods: After transfecting HK2 cells with short hair RNA (shRNA), shTRAF1 gene silencing model was established. The cells were divided into shRNA group and shNC group. For kidney injury model, we used hypoxia/reoxygenation to establish H/R cell lines. MTT assay was used to determine cell viability. PI/FITC staining was used to determine cell apoptosis. The genes expressions were determined by RT-qPCR and western blotting, respectively. The concentration of MDA, SOD, iNOS and LDH was determined by ELISA.

Results: The results of RT-qPCR and western blotting assay revealed that TRAF1 upregulated expression in AKI model cells. The results of MTT assay revealed that shRNA group exhibited significantly higher cell viability and lower cell apoptosis compared with the control group in H/R HK2 cells. In addition, TRAF1 downregulated expression inhibits oxidative stress response in H/R treated HK2 cell. Mechanically, TRAF1 deficiency protects HK2 cell via inhibiting p38-MAPK pathway.

Conclusions: Our study suggests that TRAF1 could be a target in kidney injury treatment.

Keywords

TRAF1

AKI

Cell apoptosis

H/R injury

p38 MAPK pathway

Figures

Fig. 1.

Previous article in this issue

Next article in this issue

Fig. 1.

TRAF1 is elevated in renal tubular cells induced by hypoxia/reoxygenation. (A&B) RT-qPCR and western blotting analysis the expression of TRAF1 in hypoxia/reoxygenation injury HK2 cell. Error bars represent data from three independent experiments (mean $\pm{}$ SD). **P $<$ 0.01.

1 of 4

J. Mens. Health Print ISSN 1875-6867 Electronic ISSN 1875-6859