Deportment of Orthopedic, Taizhou People's Hospital, NO.366 TaiHu Road, Taizhou, 225300, Jiangsu Province, China.
Department of Orthopedic, Jinling Hospital, the first School of Clinical Medicine, Southern Medical University, Nanjing, 210000, Jiangsu Province, China.
J Surg Res. 2021 Oct;266:148-159. doi: 10.1016/j.jss.2021.03.046. Epub 2021 May 12.
The aim of this study was to investigate the mechanism of hydrogen gas on hind limb IR injury.
Male C57BL/6 mice were randomly divided into three groups: sham group (Sham), ischemia-reperfusion group (IR), IR plus H inhalation group (IR + H). IR was induced by interrupting hind limb blood flow for 3h, followed by 4h of reperfusion, and H was administered by inhalation throughout the reperfusion process. Our data show that H 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).
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.
本研究旨在探讨氢气对后肢 IR 损伤的作用机制。
雄性 C57BL/6 小鼠随机分为三组：假手术组（Sham）、缺血再灌注组（IR）、IR 加氢气吸入组（IR+H）。通过阻断后肢血流 3h 后再灌注 4h 诱导 IR，整个再灌注过程中通过吸入氢气。我们的数据表明，与 IR 组相比，氢气吸入可显著减少梗死相关组织体积（P<0.05），减轻形态损伤程度（P<0.05），抑制氧化应激损伤水平（P<0.05）。在探索潜在机制时，我们发现氢气可显著减轻 IR 诱导的内质网应激和细胞凋亡程度（P<0.05）。此外，氢气通过调节磷酸化 c-Jun N 末端激酶（JNK）信号通路（P<0.05）显著抑制 IR 损伤。
综上所述，这些结果揭示了氢气通过减轻氧化应激、损伤内质网应激和细胞凋亡以及调节 JNK 信号通路来减轻小鼠后肢缺血再灌注损伤的保护作用。
