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BioMed Research International
Volume 2015, Article ID 508101, 8 pages
Research Article

Role of Exogenous Hsp72 on Liver Dysfunction during Sepsis

1Graduate Institute of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
2Department of Physiology, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan
3Graduate Institute of Marine Biotechnology, National Dong Hwa University, Pingtung 97401, Taiwan
4Center of Teaching and Research, Kaohsiung Municipal Ta-Tung Hospital, Kaohsiung Medical University Hospital, Kaohsiung 80145, Taiwan
5Department of Pediatrics, Kaohsiung Medical University Hospital, Kaohsiung 807, Taiwan
6Department of Pediatrics, Changhua Christian Hospital, Changhua 500, Taiwan

Received 16 April 2015; Revised 2 June 2015; Accepted 3 June 2015

Academic Editor: Roland S. Croner

Copyright © 2015 Tsen-Ni Tsai et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


This study examined the role of exogenous heat shock protein 72 (Hsp72) in reversing sepsis-induced liver dysfunction. Sepsis was induced by cecal ligation and puncture. Liver function was determined on the basis of the enzymatic activities of serum glutamate oxaloacetate transaminase (GOT) and glutamate pyruvate transaminase (GPT). Apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labeling staining. B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3 and caspase-9, and cleaved poly (ADP-ribose) polymerase (PARP) protein expressions were analyzed using Western blotting. Results showed GOT and GPT levels increased during sepsis, and levels were restored following the administration of human recombinant Hsp72 (rhHsp72). Increased liver tissue apoptosis was observed during sepsis, and normal apoptosis resumed on rhHsp72 administration. The Bcl-2/Bax ratio, cleaved caspase-3, caspase-9, and PARP protein expressions in the liver tissues were upregulated during sepsis and normalized after rhHsp72 treatment. We conclude that, during sepsis, exogenous Hsp72 restored liver dysfunction by inhibiting apoptosis via the mitochondria-initiated caspase pathway.