Thioredoxin relieves lipopolysaccharide‑induced acute kidney injury in mice by reducing inflammation, oxidative stress and apoptosis
- Jingjing Wang
- Wenjuan Zhang
- Guoyuan Lu
Affiliations: Department of Nephrology, Changzhou Fourth People's Hospital, Changzhou, Jiangsu 213000, P.R. China, Department of Nephrology, First Affiliated Hospital of Suzhou University, Suzhou, Jiangsu 215000, P.R. China
- Published online on: April 15, 2021 https://doi.org/10.3892/etm.2021.10061
Copyright: © Wang
et al. This is an open access article distributed under the
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Acute kidney injury (AKI) is a serious disease with rapid onset and a high mortality rate. It is therefore particularly important to identify a suitable method for treating AKI. Thioredoxin (Trx) is a potent anti‑inflammatory and anti‑oxidant protein that is prevalent in living organisms. The aim of the present study was to facilitate the clinical treatment of AKI via the study of Trx. Lipopolysaccharide (LPS) was used to construct an AKI model in mice and the mice were pre‑treated with Trx to examine its effect on AKI. In addition, human renal tubular epithelial HK‑2 cells were cultured and stimulated with Trx to examine its effect on inflammation, levels of oxidative stress and apoptosis in the HK‑2 cells. The NF‑κB signaling pathway is a classical inflammation‑related pathway and the mechanism of Trx was investigated by evaluating the association between Trx and the NF‑κB signaling pathway. Trx treatment reduced LPS‑induced levels of inflammation, oxidative stress and apoptosis in the HK‑2 cells. The activity of NF‑κB signaling pathway was increased in LPS‑induced HK‑2 cells, while Trx treatment effectively reduced NF‑κB signaling pathway activity. In addition, Trx treatment significantly reduced LPS‑induced mouse AKI in vivo, which was characterized by a decrease in inflammatory factors in mouse serum, a decrease in AKI‑associated molecules in mouse urine and a decrease in oxidative stress levels in mouse kidney tissue samples. Trx treatment reduced inflammation, levels of oxidative stress and apoptosis in HK‑2 cells by inhibiting the NF‑κB signaling pathway, thereby alleviating LPS‑induced mouse AKI.