Hydrogen Therapy Protects Liver During Surgery in Pigs
- Authors
- Yan-Song Ge, Qian-Zhen Zhang, Hui Li, Ge Bai, Zhi-Hui Jiao, Hong-Bin Wang
- Journal
- Hepatobiliary & Pancreatic Diseases International
- Year
- 2018
- DOI
- 10.1016/j.hbpd.2018.12.001
- Study Type
- Pig
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Hepatic Ischemia-Reperfusion Injury
- Body System
- Hepatic
TL;DR
Treating pigs with hydrogen-rich saline helped protect their livers from damage during surgery and improved liver healing.
Key Finding
Hydrogen-rich saline reduced liver damage from surgery and blood flow interruption by decreasing harmful oxidative stress, lowering inflammatory markers, and promoting liver cell regeneration in pigs.
Summary
Researchers tested hydrogen-rich saline (a salt water solution containing dissolved hydrogen gas) in pigs undergoing liver surgery to see if it could reduce damage from temporary loss of blood flow to the liver. The treatment reduced markers of cell damage, lowered inflammatory chemicals in the blood, and improved the liver's ability to heal and regenerate after surgery.
Practical Takeaway
This is an animal study in pigs, so results cannot be directly applied to humans yet. While the findings suggest hydrogen-rich saline may protect liver tissue during surgical stress, human clinical trials would be needed to determine if similar benefits occur in people undergoing liver surgery.
Abstract
Background Hydrogen-rich saline (HRS) has antioxidative, anti-inflammatory and anti-apoptotic properties. We investigated the effects of hydrogen on hepatic ischemia-reperfusion (I/R) and laparoscopic hepatectomy in swine. Methods Twenty-one healthy Bama miniature pigs were randomly divided into the sham group, ischemia-reperfusion injury (IRI) group, HRS-5 (5 mL/kg) group, and HRS-10 (10 mL/kg) group. HRS was injected through the portal vein 10 min before reperfusion and at postoperative day 1, 2 and 3. The roles of HRS on oxidative stress, inflammatory response and liver regeneration were studied. Results Compared with the IRI group, HRS treatment attenuated oxidative stress by increasing catalase activity and reducing myeloperoxidase. White blood cells in the HRS-10 group were reduced compared with the IRI group (P < 0.01). In the HRS-10 group, interleukin-1 beta, interleukin-6 and tumor necrosis factor alpha, C-reactive protein and cortisol were downregulated, whereas interleukin-10 was upregulated. In addition, HRS attenuated endothelial cell injury and promoted the secretion of angiogenic cytokines, including vascular endothelial growth factor, angiopoietin-1 and angiopoietin-2. HRS elevated the levels of hepatocyte growth factor, Cyclin D1, proliferating cell nuclear antigen, Ki-67 and reduced the secretion of transforming growth factor-beta. Conclusions HRS treatment may exert a protective effect against I/R and hepatectomy-induced hepatic damage by reducing oxidative stress, suppressing the inflammatory response and promoting liver regeneration.