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Biomed Rep. 2017 May;6(5):525-531. doi: 10.3892/br.2017.891. Epub 2017 Apr 11.

Expression of tubulin folding cofactor B in mouse hepatic ischemia-reperfusion injury.

Author information

1
Department of Hepatobiliary Surgery and Laboratory, Affiliated Hospital of Guilin Medical University, Guilin, Guangxi 541001, P.R. China.
2
Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, The Second Hospital of Dalian Medical University, Dalian, Liaoning 116027, P.R. China.

Abstract

The aim of the present study was to investigate the association between tubulin folding cofactor B (TBCB) expression and ischemia-reperfusion injury (IRI) in mice. A total of 48 C57BL/6 mice were randomly divided into a control group (Sham, n=6) and an ischemia-reperfusion group (n=42). The ischemia-reperfusion group was further divided into 6 subgroups as per different times after reperfusion (2, 4, 6, 8, 12 and 24 h), with 7 mice per subgroup. A hepatic IRI model was established in mice by clamping the hepatic hilum. Morphology, serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α), and the expression level of TBCB were detected. Compared with the control group, the livers from the ischemia-reperfusion group were significantly changed, particularly at 12 h following ischemia-reperfusion, with obvious hepatic cell degeneration and necrosis. The ALT, AST, IL-6 and TNF-α levels in the sera of the mice in the hepatic ischemia-reperfusion group were increased at all time points following ischemia-reperfusion, and were the highest at 12 h, demonstrating statistically significant differences when compared with the control group (P<0.05). Furthermore, the expression levels of TBCB, TNF-α and IL-6 were significantly increased at all time-points following ischemia-reperfusion, and were the most significant at 12 h. At 24 h following ischemia-reperfusion, the expression levels had decreased. The present study indicated that TBCB expression is associated with TNF-α and IL-6 expression levels in mice with hepatic ischemia-reperfusion, and may be key in the development of liver injury during ischemia-reperfusion in mice.

KEYWORDS:

cell microtubule; cytoskeleton; ischemia-reperfusion injury; tubulin folding cofactor B

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