Hydrogen-Rich Saline Ameliorates Hepatic Ischemia-Reperfusion Injury Through Regulation of Endoplasmic Reticulum Stress and Apoptosis.
Dig Dis Sci
; 62(12): 3479-3486, 2017 12.
Article
em En
| MEDLINE
| ID: mdl-29086332
OBJECTIVE: To evaluate the effect of hydrogen-rich saline (HS) on hepatic ischemia-reperfusion (I/R) injury. METHODS: Forty 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. RESULTS: Serum 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. CONCLUSION: The protective effect of HS can be attributed to ER stress and apoptosis inhibition.
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Base de dados:
MEDLINE
Assunto principal:
Cloreto de Sódio
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Traumatismo por Reperfusão
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Apoptose
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Insuficiência Hepática
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Estresse do Retículo Endoplasmático
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Hidrogênio
Tipo de estudo:
Evaluation_studies
Limite:
Animals
Idioma:
En
Ano de publicação:
2017
Tipo de documento:
Article