Hydrogen Water Protects Intestines from Surgery-Related Injury in Mice
- Authors
- Weifeng Yao, Xiaoyu Lin, Xue Han, Lanfen Zeng, Anshun Guo, Yu Guan, Ziqing Hei, Jianpei Liu, Pinjie Huang
- Journal
- Bioscience Reports
- Year
- 2019
- DOI
- 10.1042/BSR20191043
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Intestinal Ischemia-Reperfusion Injury
- Body System
- Gastrointestinal
TL;DR
Hydrogen-rich saline (HRS) may protect the intestines from damage due to temporary loss and restoration of blood supply by regulating certain microRNA molecules.
Key Finding
Hydrogen-rich saline reduced intestinal damage from ischemia/reperfusion injury in mice by lowering levels of miR-199a-3p, which activated cell survival pathways and prevented intestinal cell death.
Summary
Researchers studied how hydrogen-rich saline (a salt solution containing dissolved hydrogen) protects the intestines from damage caused by temporarily cutting off blood flow and then restoring it. Using mice, they found that hydrogen-rich saline reduced intestinal injury and cell death, and they identified a specific molecular switch called miR-199a-3p that appears to be responsible for this protective effect by activating survival pathways in intestinal cells.
Practical Takeaway
This is an early-stage animal study that identifies a potential mechanism for how hydrogen water might protect intestinal tissue from injury. However, these findings are from mice only, and it remains unclear whether the same protective effect would occur in humans or with the amounts of hydrogen in commercially available hydrogen water products. More research in humans would be needed before drawing conclusions about practical health benefits.
Abstract
Abstract Background: Hydrogen-rich saline (HRS) has been proven effective against ischemia/reperfusion (I/R) injury. However, knowledge on the underlying signaling events remain poor. Having recent highlight of microRNAs (miRNAs) in mediating intestinal I/R injury, we hypothesized that HRS may protect intestine against I/R injury by regulating miRNAs. Method: Mice were given intraperitoneal injection of saline or HRS once daily for five consecutive days before undergoing intestinal I/R that was induced by 60-min ischemia followed by 180-min reperfusion of superior mesenteric artery. The intestine was collected for histopathological assay, miRNA microarray profiling, Real-Time PCR, and Western blotting. Next, miR-199a-3p mimics or inhibitors were transfected into IEC-6 cells to explore the relationship between HRS treatment and miR-199a-3p. Results: I/R-induced mucosal injury and epithelial cells apoptosis were attenuated by HRS pretreatment. A total of 64 intestinal I/R-responsive miRNAs were altered significantly by HRS pretreatment, in which we validated four novel miRNAs with top significance by Real-Time PCR, namely miR-199a-3p, miR-296-5p, miR-5126, and miR-6538. Particularly, miR-199a-3p was drastically increased by I/R but reduced by HRS. Computational analysis predicts insulin-like growth factor (IGF)-1, mammalian target of rapamycin (mTOR), and phosphoinositide-3-kinase (PI3K) regulatory subunit 1 as targets of miR-199a-3p, suggesting involvement of the pro-survival pathway, IGF- 1/PI3K/Akt/mTOR. In in vitro experiment, HRS treatment reduced miR-199a-3p level, increase IGF-1, PI3K and mTOR mRNA expression, restore IEC-6 cells viability, and this protective effects were reversed under miR-199a-3p mimics treatment. Conclusion: Collectively, miR-199a-3p may serve a key role in the anti-apoptotic mechanism of HRS that contributes to its protection of the intestine against I/R injury.