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Hydrogen-Rich Saline Ameliorates Hepatic Ischemia-Reperfusion Injury Through Regulation of Endoplasmic Reticulum Stress and Apoptosis

Authors
  • Lu, Zhiyuan1
  • Lin, Yanzhu2
  • Peng, Bo3
  • Bao, Zhen3
  • Niu, Kexin3
  • Gong, Jin3
  • 1 Sun Yat-Sen University, Department of Oral and Maxillofacial Surgery, The First Affiliated Hospital, Guangzhou, People’s Republic of China , Guangzhou (China)
  • 2 Sun Yat-Sen University Cancer Center, State Key Laboratory of Oncology in Southern China, Sun Yat-Sen University, Department of Radiation Oncology, Guangzhou, People’s Republic of China , Guangzhou (China)
  • 3 Jinan University, Department of General Surgery, The First Affiliated Hospital, Guangzhou, 510632, People’s Republic of China , Guangzhou (China)
Type
Published Article
Journal
Digestive Diseases and Sciences
Publisher
Springer-Verlag
Publication Date
Oct 30, 2017
Volume
62
Issue
12
Pages
3479–3486
Identifiers
DOI: 10.1007/s10620-017-4811-8
Source
Springer Nature
Keywords
License
Yellow

Abstract

ObjectiveTo evaluate the effect of hydrogen-rich saline (HS) on hepatic ischemia-reperfusion (I/R) injury.MethodsForty rats were randomly allocated into five groups: one sham group (control group), one group treated with 20 min of ischemia and normal saline (NS; I/R1 + NS group), one group treated with 20 min of ischemia and HS (I/R1 + HS group), one group treated with 60 min of ischemia and NS (I/R2 + NS group), and one group treated with 60 min of ischemia and HS (I/R2 + HS group). After reperfusion for 6 h, hepatic function, oxidative stress, pathological changes, and apoptosis of hepatic cells were evaluated. Furthermore, the expression levels of endoplasmic reticulum (ER) stress-associated proteins were identified.ResultsSerum ALT and AST levels and tissue MDA content in the I/R + HS groups were significantly lower than those in the I/R + NS groups. Pathological changes were also significantly ameliorated in the HS groups compared with those in the NS groups. Moreover, HS appeared to significantly attenuate hepatic I/R-induced ER stress responses, as indicated by the decreased expression of C/EBP homologous protein, protein-kinase-RNA-like ER kinase, and inositol-requiring protein-1α, as well as the increased expression of GRP78 proteins. Finally, the levels of apoptotic markers such as caspase-3 and TUNEL-positive cells were significantly lower in the HS groups than in the NS control groups, whereas the level of Bcl2 protein increased in the HS groups.ConclusionThe protective effect of HS can be attributed to ER stress and apoptosis inhibition.

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