Hydrogen Therapy Protects Heart During Sepsis in Mice Study

Authors
Journal
BMC Anesthesiology
Year
DOI
10.1186/s12871-024-02462-4
Study Type
Mouse
Outcome
Positive
Peer Reviewed
Yes
Country
China
Health Condition
Sepsis
Body System
Cardiovascular

TL;DR

Breathing in molecular hydrogen gas significantly improves survival and reduces heart damage in mice with sepsis-induced heart problems, potentially by enhancing the cell's cleanup processes.

Key Finding

Molecular hydrogen inhalation improved survival rates and reduced heart damage in septic mice, with the protective effect dependent on activating a cellular cleanup process called autophagy.

Summary

This study tested whether inhaling molecular hydrogen gas could protect the hearts of mice with sepsis (a life-threatening infection). Researchers found that mice breathing hydrogen had better survival rates, less heart damage, and lower levels of a protein that indicates heart injury. The protective effect appeared to work by activating a cellular cleanup process called autophagy. When researchers blocked autophagy with a drug, hydrogen's protective benefits disappeared.

Practical Takeaway

This early animal study suggests hydrogen gas may help protect the heart during severe infection, but it is only a mouse study and much more research—including human trials—would be needed before any health claims could be made. The findings are preliminary and should not be interpreted as evidence that hydrogen can treat sepsis or heart disease in people.

Abstract

Background: Approximately 40 to 60% of patients with sepsis develop sepsis-induced cardiomyopathy (SIC), which is associated with a substantial increase in mortality. We have found that molecular hydrogen (H2) inhalation improved the survival rate and cardiac injury in septic mice. However, the mechanism remains unclear. This study aimed to explore the regulatory mechanism by which hydrogen modulates autophagy and its role in hydrogen protection of SIC. Methods: Cecal ligation and puncture (CLP) was used to induce sepsis in adult C57BL/6J male mice. The mice were randomly divided into 4 groups: Sham, Sham + 2% hydrogen inhalation (H2), CLP, and CLP + H2 group. The 7-day survival rate was recorded. Myocardial pathological scores were calculated. Myocardial troponin I (cTnI) levels in serum were detected, and the levels of autophagy- and mitophagy-related proteins in myocardial tissue were measured. Another four groups of mice were also studied: CLP, CLP + Bafilomycin A1 (BafA1), CLP + H2, and CLP + H2 + BafA1 group. Mice in the BafA1 group received an intraperitoneal injection of the autophagy inhibitor BafA1 1 mg/kg 1 h after operation. The detection indicators remained the same as before. Results: The survival rate of septic mice treated with H2 was significantly improved, myocardial tissue inflammation was improved, serum cTnI level was decreased, autophagy flux was increased, and mitophagy protein content was decreased (P < 0.05). Compared to the CLP + H2 group, the CLP + H2 + BafA1 group showed a decrease in autophagy level and 7-day survival rate, an increase in myocardial tissue injury and cTnI level, which reversed the protective effect of hydrogen (P < 0.05). Conclusion: Hydrogen exerts protective effect against SIC, which may be achieved through the promotion of autophagy and mitophagy.