Hydrogen Therapy Protects Kidneys After Liver Transplant Surgery
- Authors
- Hongyin Du, Mingwei Sheng, Li Wu, Yamin Zhang, Dongjing Shi, Yiqi Weng, Rubin Xu, Wenli Yu
- Journal
- Transplantation
- Year
- 2015
- DOI
- 10.1097/TP.0000000000001052
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Kidney Injury
- Body System
- Renal
TL;DR
Hydrogen-rich saline (HRS) helps protect against kidney damage following liver transplantation by reducing cell death and influencing a cell's waste disposal system.
Key Finding
Hydrogen-rich saline significantly reduced kidney damage and improved kidney function in rats after liver transplantation, partly by activating a cellular cleanup process and reducing cell death.
Summary
This rat study tested whether hydrogen-rich saline (salt water containing dissolved hydrogen) could prevent kidney damage that sometimes occurs after liver transplants. Researchers found that hydrogen-rich saline reduced kidney damage, improved kidney function, and lowered harmful molecules called oxidative stress. The protective effect appeared to work by activating a cellular cleanup process called autophagy and reducing cell death.
Practical Takeaway
This is early-stage research in rats only, so results cannot yet be applied to humans. The study suggests hydrogen-rich saline may warrant further investigation as a potential treatment to protect kidneys during liver transplants, but human clinical trials would be needed to determine if it actually works in transplant patients.
Abstract
Background: Acute kidney injury (AKI) impacts the survival of liver transplant recipients severely. To date, the related mechanism and effective therapy have not been rigorously explored. The present study aimed to explore the role of p53-mediated autophagy in the protective effect of hydrogen-rich saline (HRS) on AKI after orthotropic liver transplantation (OLT). Methods: Adult male Sprague-Dawley rats were randomly allocated into four groups: sham, OLT, OLT with HRS (6 ml/kg) pretreatment (HS), OLT with HRS and chloroquine pretreatment (60 mg/kg) group (CQ). All the samples were collected 6 hours after reperfusion. The renal function and oxidative stress level were measured by biochemical and histopathologic examinations. The formation of autophagosome was observed by transmission electron microscopy. The apoptotic rate was determined by terminal deoxynucleotide transferase-mediated deoxyuridine triphosphate nick-end labeling analysis. The expression of caspase-3, cytochrome c, p53, damage-regulated autophagy modulator, Becline-1, microtubule-associated protein light 3-II, p62, lysosome-associated membrane protein-2, and the phosphorylation of p53 were assayed by western blot assay. Results: Compared with the OLT group, HRS dramatically attenuated the histopathologic damage, restored the renal function, and decreased the oxidative stress level. Simultaneously, HRS significantly ameliorated apoptosis by decreasing the apoptotic rate and inhibiting the expression of caspase-3 and cytochrome c in rats subjected to OLT. The expression of Becline-1 and microtubule-associated protein light 3-II were upregulated with the inhibition of p62 and lysosome-associated membrane protein-2. The inhibition of autophagy by chloroquine counteracted the renoprotective effects of HRS. Conclusions: HRS is able to protect against AKI after liver transplantation partly by reducing apoptosis, which is possibly involved in the modulation of p53-mediated autophagy.