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Protective Effect of Hydrogen Gas on Mouse Hind Limb Ischemia-Reperfusion Injury
Jian Tong1, Yu Zhang2, Pan Yu3
1Deportment of Orthopedic, Taizhou People's Hospital, NO.366 TaiHu Road, Taizhou, 225300, Jiangsu Province, China.
Background:
The aim of this study was to investigate the mechanism of hydrogen gas on hind limb IR injury.
Methods:
Male C57BL/6 mice were randomly divided into three groups: sham group (Sham), ischemia-reperfusion group (IR), IR plus H2 inhalation group (IR + H2). IR was induced by interrupting hind limb blood flow for 3h, followed by 4h of reperfusion, and H2 was administered by inhalation throughout the reperfusion process. Our data show that H2 inhalation could significantly decrease the infarct-affected tissue volume (P < 0.05), attenuate the degree of morphological injury (P < 0.05), and suppress the level of oxidative stress damage (P < 0.05), compared with the IR group. In exploring the underlying mechanisms, we found that hydrogen could markedly mitigate the degree of IR-induced ER stress and apoptosis (P < 0.05). Additionally, hydrogen could markedly inhibit the IR injury by modulating the phosphorylated c-Jun N-terminal kinase (JNK) signaling pathway (P < 0.05).
Conclusions:
Taken together, these results revealed the protective effect of hydrogen gas on hind limb ischemia reperfusion injury on mice by attenuating oxidative stress, impairing ER stress and apoptosis, and its ability to modulate JNK signaling pathway.
Insights
Hydrogen gas inhalation protects against hind limb ischemia reperfusion injury. It reduces tissue damage, oxidative stress, ER stress, and apoptosis by modulating the JNK pathway.
Area of Science:
- Biomedical Science
- Physiology
- Molecular Biology
Background:
- Ischemia reperfusion (IR) injury is a significant clinical challenge.
- Hind limb IR injury models are crucial for studying therapeutic interventions.
- Understanding the protective mechanisms of hydrogen gas is of therapeutic interest.
Purpose of the Study:
- To investigate the protective mechanisms of hydrogen gas against hind limb ischemia reperfusion (IR) injury.
- To elucidate the role of hydrogen in mitigating oxidative stress, ER stress, and apoptosis.
- To explore the modulation of the JNK signaling pathway by hydrogen.
Main Methods:
- Male C57BL/6 mice were divided into sham, IR, and IR + H2 groups.
- Hind limb ischemia was induced for 3 hours, followed by 4 hours of reperfusion.
- Hydrogen gas was administered via inhalation during the reperfusion period.
Main Results:
- Hydrogen inhalation significantly reduced infarct volume and morphological injury in IR mice (P < 0.05).
- Hydrogen suppressed IR-induced oxidative stress, ER stress, and apoptosis (P < 0.05).
- Hydrogen modulated the phosphorylated JNK signaling pathway, inhibiting IR injury (P < 0.05).
Conclusions:
- Hydrogen gas demonstrates a protective effect against hind limb IR injury in mice.
- The protective mechanisms involve attenuating oxidative stress, ER stress, and apoptosis.
- Hydrogen modulates the JNK signaling pathway, contributing to its therapeutic benefit.
