Hydrogen Water Protects Kidneys from Damage After Blood Flow Loss
- Authors
- Jing Chen, Han Zhang, Jiachang Hu, Yulu Gu, Ziyan Shen, Linghan Xu, Xueqi Jia, Xiaoyan Zhang, Xiaoqiang Ding
- Journal
- Frontiers in Pharmacology
- Year
- 2017
- DOI
- 10.3389/fphar.2017.00499
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Acute Kidney Injury
- Body System
- Urinary System
TL;DR
Hydrogen-rich saline (HRS) treatment helps protect against kidney damage and reduces scarring after a kidney injury caused by temporary loss of blood flow and subsequent restoration.
Key Finding
Hydrogen-rich saline reduced kidney scarring and preserved a protective protein called Klotho in mice with acute kidney injury caused by temporary loss of blood flow.
Summary
Researchers tested whether hydrogen-rich saline (salt water containing dissolved hydrogen gas) could protect mouse kidneys from damage caused by temporarily cutting off blood flow and then restoring it. They found that mice treated with hydrogen-rich saline had less scarring in their kidneys, better kidney function, and higher levels of a protective protein called Klotho compared to untreated mice with the same injury.
Practical Takeaway
This early-stage mouse study suggests hydrogen-rich saline may help prevent kidney scarring after acute injury, but much more research is needed before any conclusions can be drawn for human health. The findings are preliminary and limited to laboratory animals, so it's too early to know whether these results would apply to people.
Abstract
Purpose: Acute kidney injury (AKI) is a prominent risk factor for the development of chronic kidney disease (CKD). To date, the related mechanism and effective therapy have not been rigorously explored. The present study aims to investigate the reno-protection of hydrogen-rich saline (HRS) against ischemia/reperfusion (IR)-induced AKI. Methods: Adult male C57 mice were randomly allocated into three groups: Sham, IR, IR+HRS. Renal IR injury model was generated via 35 min occlusion of bilateral kidney pedicles, and then, mice were administered with different treatments intraperitoneally in various groups. After 14- or 28-day treatment, mice were perfused and the kidneys were collected following reperfusion. Many proteins were detected by western blots, including renal fibrotic proteins [a-smooth muscle actin (a-SMA), collagen I (Col I)], Klotho, the methylation of Klotho, damage-regulated autophagy modulator (Beclin-1), and microtubule-associated protein light 3-II (LC3-II). Finally, the levels of serum blood urea nitrogen (BUN) and creatinine (Cr) were measured to investigate the renal function. Results: Histological data showed that the HRS treatment significantly decreased the fibrosis in renal tissues when compared with the IR group, and both of BUN and Cr were lower in the HRS group than IR group (8.9 ± 0.6 vs. 9.9 ± 0.1 mmol/l, 51 ± 6.5 vs. 60 ± 5.8 μmol/l) (P < 0.05). The expression of fibrotic markers, a-SMA and Col I, showed a robust increase in IR injury models than the Sham group, which was consistent with the result of Trichrome staining. However, the levels of a-SMA and Col I expression were sharply decreased in the IR+HRS group (P < 0.05). IR injury also enhanced LC3-II and Beclin-1 expression, but decreased Klotho level. The Klotho level was alleviated by HRS, but LC3-II and Beclin-1 were starkly enhanced in HRS group (P < 0.05). Conclusion: HRS showed a protective effect in the prevention of renal injury and could inhibit renal fibrosis after IR injury in mice. This role of HRS might be exerted via retaining Klotho expression and activating autophagy in the kidney.