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.
Keywords: ER stress; Hydrogen gas; Ischemia reperfusion injury; JNK pathway; Oxidative stress.
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