Zou Ji-He, Qiao Wei-Li, Wang Guang-Ming, Ma Hong-Ji, Qi You-Jian, Sun Hong, Yan Chang-Dong
Department of Physiology, Xuzhou Medical College, Xuzhou 221002, China.
Sheng Li Xue Bao. 2012 Feb 25;64(1):27-32.
The present study aimed to investigate the protective effect and mechanism of hydrogen sulfide donor NaHS administration against gastric mucosal injury induced by gastric ischemia-reperfusion (GI-R) in rats. GI-R injury was induced by clamping the celiac artery of adult male SD rats for 30 min and followed by reperfusion for 1 h. The rats were randomly divided into sham group, GI-R group, NaHS group, glibenclamide group and pinacidil group. Gastric mucosal damage was analyzed with macroscopic injured area, deep damage was assessed with histopathology scores, and the hydrogen sulfide concentration in plasma was determined by colorimetric method. The results showed that pretreatment of NaHS significantly reduced the injured area and deep damage of the gastric mucosa induced by GI-R. However, NaHS did not significantly alter the levels of hydrogen sulfide in plasma 14 d after NaHS administration. The gastric protective effect of NaHS during reperfusion could be attenuated by glibenclamide, an ATP-sensitive potassium channel (K(ATP)) blocker. However, K(ATP) opener pinacidil inhibited the GI-R-induced injury. These results suggest that exogenous hydrogen sulfide plays a protective role against GI-R injury in rats possibly through modulation of K(ATP) channel opening.
本研究旨在探讨硫化氢供体硫氢化钠(NaHS)给药对大鼠胃缺血-再灌注(GI-R)诱导的胃黏膜损伤的保护作用及机制。通过夹闭成年雄性SD大鼠的腹腔动脉30分钟,然后再灌注1小时来诱导GI-R损伤。将大鼠随机分为假手术组、GI-R组、NaHS组、格列本脲组和吡那地尔组。用宏观损伤面积分析胃黏膜损伤情况,用组织病理学评分评估深度损伤,并通过比色法测定血浆中的硫化氢浓度。结果显示,NaHS预处理显著降低了GI-R诱导的胃黏膜损伤面积和深度损伤。然而,NaHS给药后14天,血浆中硫化氢水平无显著变化。格列本脲(一种ATP敏感性钾通道(K(ATP))阻滞剂)可减弱NaHS在再灌注期间的胃保护作用。然而,K(ATP)开放剂吡那地尔可抑制GI-R诱导的损伤。这些结果表明,外源性硫化氢可能通过调节K(ATP)通道开放对大鼠GI-R损伤发挥保护作用。