Hydrogen Therapy Protects Elderly Kidneys from Surgical Damage

Authors
Journal
International Journal of Clinical and Experimental Pathology
Year
Study Type
Rat
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Acute Kidney Injury
Body System
Renal

TL;DR

Hydrogen-rich saline helps protect the kidneys from damage caused by temporary loss and restoration of blood flow in aged rats.

Key Finding

Hydrogen-rich saline reduced kidney damage and improved kidney function in aged rats experiencing ischemia-reperfusion injury by decreasing oxidative stress (cellular damage from harmful molecules) and increasing expression of a protective protein called heme oxygenase-1.

Summary

This study tested whether hydrogen-rich saline could protect kidney function in aged rats that experienced a temporary loss of blood flow followed by blood flow restoration (a condition called ischemia-reperfusion injury). Researchers found that hydrogen-rich saline reduced markers of cellular damage, improved kidney function measurements, and activated protective proteins in the kidney compared to regular saline.

Practical Takeaway

This is an early-stage animal study in rats, so results cannot yet be applied to humans. The findings suggest hydrogen-rich saline may have potential to protect kidneys during ischemic events, but human clinical trials would be needed to determine if this benefit translates to elderly patients undergoing procedures that restrict kidney blood flow.

Abstract

Objective: Oxygen free radicals (ROS) are considered to be one of the important factors involved in the pathophysiology of aged renal ischemia-reperfusion (I/R) injury. Hydrogen gas has been reported to alleviate I/R injury by scavenging free radicals. The aim of this study was to evaluate the effect of hydrogen-rich saline (HRS) on renal I/R injury in aged rats. Materials and methods: A rat model of renal I/R injury was induced by 45-min occlusion of the bilateral renal pedicles and 24-h reperfusion. Physiological saline or HRS (8 ml/kg) was administered intraperitoneally 5 min before reperfusion. Parameters indicating renal function (blood urea nitrogen (BUN) and serum creatinine (SCr)) and those indicating oxidative stress (tissue levels of malondialdehyde (MDA) and 8-hydroxy-deoxyguanosine (8-OHdG), tissue activities of superoxide dismutase (SOD), and tissue expression of heme oxygenase-1 (HO-1)) were measured. Results: After I/R injury, BUN, SCr, tissue levels of MDA and 8-OHdG, and gene expression of HO-1 were all significantly increased while tissue activities of SOD were significantly decreased. HRS reversed these changes, with the exception of HO-1 expression, which was increased further, and improved renal morphology. Conclusions: HRS improves the renal response to I/R in aged rats, possibly by reducing oxidative stress and upregulating HO-1 gene expression.