Related Experiment Video
Updated: May 3, 2026
Generation of a Rat Model of Acute Liver Failure by Combining 70% Partial Hepatectomy and Acetaminophen
Published on: November 27, 2019
Hydrogen-rich saline attenuates postoperative liver failure after major hepatectomy in rats
Yun Chang Tan1, Feng Xie2, Hui Lu Zhang3
1General Surgery Department, Jiujiang University Clinical Medical College, Jiujiang university hospital, 332000 Jiujiang City, China; Department of Special Treatment, Eastern Hepatobiliary Surgery Hospital, Second Military Medical University, 200438 Shanghai, China.
Background/Aims:
A major hepatectomy occasionally lead to acute liver failure and death. We demonstrated the anti-oxidative and anti-inflammatory effects and functional mechanisms of hydrogen-rich saline (HS), a novel antioxidant, on an experimental model of rats after a partial hepatectomy (PH).
Methods:
The rats underwent a 90% hepatectomy. HS was given intraperitoneally after the operation and every 8hours after.
Results:
HS markedly improved the survival rate of two experimental groups after the massive hepatectomy and inhibited increases in serum levels of TBIL, DBIL, ALT and AST. The histopathological analysis demonstrated that HS attenuated inflammatory changes in the liver. HS administration markedly lowered the massive hepatectomy induced elevation of the serum hyaluronic acid (HA) concentrations. HS inhibited the formation of one of the markers of oxidative damage, malondialdehyde (MDA), and increased the activities of superoxide dismutase (SOD) in liver tissue. In the HS-treated group, increases in inflammatory cytokines, such as TNF-α, IL-6 and HMGB-1, were inhibited in the liver tissue. The NF-κB p65 staining revealed that HS inhibited the activation of the transcription factor nuclear factor kappa B (NF-kB).
Conclusions:
HS attenuates the massive hepatectomy induced liver injury not only by attenuating oxidative damage, but also by reducing the production of inflammatory cytokines, such as TNF-α, IL-6 and HMGB-1, in part through the inhibition of NF-kB activation.
