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    崔洁. 外源性H2S通过抑制细胞凋亡减轻大鼠胃缺血再灌注损伤#[J]. 徐州医科大学学报, 2018, 38(2): 71-73.
    引用本文: 崔洁. 外源性H2S通过抑制细胞凋亡减轻大鼠胃缺血再灌注损伤#[J]. 徐州医科大学学报, 2018, 38(2): 71-73.
    Exogenous hydrogen sulfide attenuates gastric ischemia-reperfusion injury through apoptosis inhibition[J]. Journal of Xuzhou Medical University, 2018, 38(2): 71-73.
    Citation: Exogenous hydrogen sulfide attenuates gastric ischemia-reperfusion injury through apoptosis inhibition[J]. Journal of Xuzhou Medical University, 2018, 38(2): 71-73.

    外源性H2S通过抑制细胞凋亡减轻大鼠胃缺血再灌注损伤#

    Exogenous hydrogen sulfide attenuates gastric ischemia-reperfusion injury through apoptosis inhibition

    • 摘要: 目的 探讨H2S对大鼠胃缺血再灌注损伤的保护作用机制。方法 采用夹闭大鼠腹腔动脉30 min再灌注1 h的方法建立大鼠胃缺血再灌注损伤模型,并测定胃黏膜损伤面积。Western blotting测定胃黏膜细胞中Bcl-2, Bax以及caspase-3的表达。结果 给予NaHS(外源性H2S供体)预处理明显减少胃黏膜损伤面积。与胃缺血再灌注组相比,NaHS组Bcl-2, Bax以及caspase-3的表达显著下降。结论 NaHS能明显减轻胃缺血再灌注损伤,外源性H2S可能通过抑制胃黏膜细胞凋亡通路,发挥保护胃黏膜的作用。

       

      Abstract: Objective To investigate the protective mechanism of hydrogen sulfide (H2S) on rat gastric mucosal subjected to ischemia and perfusion. Methods Celiac artery of rates was clamped for 30 min and followed by 1 h reperfusion to induce gastric ischmia-reperfusion (GI-R) . Gastric mucosal damage was analyzed with macroscopic injured area. The expression of Bcl-2, Bax and caspase-3 in the gastric mucosal were determined by western blotting. Results Pretreatment of NaHS ( H2S exogenous donor) significantly reduced the g astric mucosal damage area induce by GI-R. Meanwhile, NaHS pretreatment inhibited the cellular Bcl-2, Bax and caspase-3 expression compared with GI-R group. Conclusion NaHS could attenuate GI-R injury . And the protective effect of exogenous H2S possibly through inh ibiting the pathway of gastric mucosal apoptosis.

       

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