内源性一氧化氮对大鼠胃黏膜缺血.再灌注损伤的保护作用
缺血.,再灌注损伤,;胃;,一氧化氮;,凋亡;,增殖;,大鼠,,缺血.,再灌注损伤,;胃;,一氧化氮;,凋亡;,增殖;,大鼠,1材料和方法,2结果,3讨论,参考文献:
摘要 :目的 研究内源性一氧化氮(nitric oxide,NO)对大鼠胃黏膜缺血.再灌注损伤的保护作用。 方法 采用大鼠胃缺血.再灌注(gastric ischemia.reperfusion,GI.R)模型(夹闭腹腔动脉30min后再灌注),通过组织学、免疫组化等方法,研究NO的前体物质左旋-精氨酸(L-arg)和NO合成酶抑制剂L-NG-硝基精氨酸甲酯(L-NAME)对缺血.再灌注后大鼠胃黏膜细胞坏死、凋亡和增殖的影响。 结果 与GI.R组相比,L-arg组胃黏膜损伤明显减轻,胃黏膜损伤面积明显缩小,凋亡细胞减少,增殖细胞增加(P<0.05);L-NAME组与GI.R组相比胃黏膜损伤明显加重,胃黏膜损伤面积明显增加,凋亡细胞增加,增殖细胞减少(P<0.05)。 结论 内源性NO对胃黏膜缺血.再灌注损伤具有保护作用。关键词 :缺血. 再灌注损伤 ;胃; 一氧化氮; 凋亡; 增殖; 大鼠
The protective role of endogenous nitric oxide in rat gastric
ischemia.reperfusion injury
QIAO Wei-li,WANG Lin,ZHANG Jian-fu,et al
(Department of Physiology,Xuzhou Medical College,Xuzhou,Jiangsu221002,China)
Abstract:Objective To investigate the protective role of endogenous nitric oxide(NO)in gastric ischemia.reperfusion(GI.R)injury of rats.Methods The GI.R model was established by clamping the celiac artery for30min and allowing reper-fusion for3h.The effects of L-arginine(NO synthesis precursor)and N-nitro-L-arginine(L-NAME,NO synthetase blocker)on gastric mucosal cellular injury,apoptosis and proliferation were observed by using histological and immunohistoche-mical methods in SD rats.Results In the L-arginine group ......
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