Magnesium Hydride Protects Gut During Shock by Reducing Inflammation
- Authors
- Changkui Cao, Pan Yu, Chengnan Chu, Zhenjie Wang, Weiqi Xu, Feng Cheng, Heng Zhao, Zhaolei Qiu
- Journal
- International Immunopharmacology
- Year
- 2024
- DOI
- 10.1016/j.intimp.2024.111688
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- China
- Health Condition
- Hemorrhagic Shock
- Body System
- Gastrointestinal
TL;DR
Magnesium hydride (MgH2) can protect the gut by reducing inflammation and preventing damage to the intestinal barrier during shock.
Key Finding
Magnesium hydride protected intestinal tissue during hemorrhagic shock in rats by suppressing the formation of neutrophil extracellular traps (immune cell structures that damage the intestinal barrier).
Summary
Researchers tested whether magnesium hydride, a material that releases hydrogen gas when taken by mouth, could protect the intestines during hemorrhagic shock (severe bleeding). Using rats and lab-grown human immune cells, they found that magnesium hydride reduced intestinal damage, improved the intestine's barrier function, and decreased inflammatory molecules in the blood. The protective effect appeared to work by reducing harmful molecules called reactive oxygen species and preventing immune cells from forming web-like traps (NETs) that damage intestinal tissue.
Practical Takeaway
This is early-stage research in animals only, so it cannot yet be applied to human health. The study suggests magnesium hydride's hydrogen-releasing properties may have protective effects on intestinal function during severe stress, but human trials would be needed to determine if this translates to real-world benefit.
Abstract
Magnesium hydride (MgH2) is a hydrogen storage material that is known for its high capacity and safety and is capable of releasing hydrogen in a controlled manner when administered orally. This release of hydrogen has been associated with a range of biological effects, including anti-inflammatory properties, antioxidant activity, and protection of the intestinal barrier. Previous research has shown that neutrophil extracellular traps (NETs) play a role in the dysfunction of the intestinal barrier in conditions such as sepsis and critical illnesses. However, it remains unclear as to whether MgH2 can protect the intestinal barrier by inhibiting NET formation, and the underlying mechanisms have yet to be elucidated. A rat model of hemorrhagic shock was created, and pretreatment or posttreatment procedures with MgH2 were performed. After 24 h, samples from the small intestine and blood were collected for analysis. In vitro, human neutrophils were incubated with either phorbol-12-myristate-13-acetate (PMA) or MgH2. Reactive oxygen species generation and the expression of key proteins were assessed. The results demonstrated that MgH2 administration led to a decrease in inflammatory cytokines in the serum and mitigated distant organ dysfunction in rats with HS. Furthermore, MgH2 treatment reversed histopathological damage in the intestines, improved intestinal permeability, and enhanced the expression of tight junction proteins (TJPs) during HS. Additionally, MgH2 treatment was found to suppress NET formation in the intestines. In vitro pretreatment with MgH2 alleviated intestinal monolayer barrier disruption that was induced by NETs. Mechanistically, MgH2 pretreatment reduced ROS production and NET formation, inhibited the activation of ERK and p38, and suppressed the expression of the PAD4 protein. These findings indicated that MgH2 may inhibit NET formation in a ROS/MAPK/PAD4-dependent manner, which reduces NET-related intestinal barrier damage, thus offering a novel protective role in preventing intestinal barrier dysfunction during HS.