TXNIP knockdown alleviates hepatocyte ischemia reperfusion injury through preventing p38/JNK pathway activation

Biochemical and Biophysical Research Communications
Yong ZhangJuan Zheng

Abstract

Hepatic ischemia and reperfusion (I/R) injury is a major cause of liver damage during liver transplantation, resection surgery, shock, and trauma. It has been reported that TXNIP expression was upregulated in a rat model of hepatic I/R injury. However, the role of TXNIP in the hepatic I/R injury is little known. In our study, we investigated the biological role of TXNIP and its potential molecular mechanism in the human hepatic cell line (HL7702 cells). Using oxygen-glucose deprivation and reoxygenation (OGD/R) to create a cell model of hepatic I/R injury, we found that the mRNA and protein expression levels of TXNIP were upregulated in HL7702 cells exposed to OGD/R. TXNIP overexpression remarkably promoted OGD/R-induced cell apoptosis and lactate dehydrogenase (LDH) release, both of which were significantly decreased by TXNIP knockdown. The production of malondialdehyde (MDA) was also increased by TXNIP overexpression, but was reduced by TXNIP knockdown. Moreover, TXNIP overexpression significantly upregulated the phosphorylation of p38 and JNK, which was remarkably inhibited by TXNIP knockdown. Additionally, p38-specific inhibitor SB203580 abrogated the effect of TXNIP overexpression on OGD/R-induced cell injury. Taken togeth...Continue Reading

Citations

Feb 26, 2019·Journal of Cellular Physiology·Yong ZhangXiaoming Lei
Feb 29, 2020·Molecules : a Journal of Synthetic Chemistry and Natural Product Chemistry·Shengtao YangChunxia Zhou
Mar 18, 2019·Apoptosis : an International Journal on Programmed Cell Death·Charles C OhPeter Reaven
Dec 29, 2020·Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS)·Sevda Altun, Harun Budak
Feb 12, 2021·International Journal of Molecular Sciences·Alison DominguesValérie Nivet-Antoine

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