Hypoxia preconditioning protects Ca(2+)-ATPase activation of intestinal mucosal cells against R/I injury in a rat liver transplantation model.
Hypoxia preconditioning protects Ca(2+)-ATPase activation of intestinal mucosal cells against R/I injury in a rat liver transplantation model.
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缺氧预处理可保护CA（2+） - 肠粘膜细胞的ATPase激活在大鼠肝移植模型中免受R/I损伤。
DOI：
10.3748/wjg.v24.i3.360
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发表时间：
2018-01-21
影响因子：
4.3
通讯作者：
Li HL
中科院分区：
文献类型：
--
作者：
Ji ZP;Li YX;Shi BX;Zhuang ZN;Yang JY;Guo S;Xu XZ;Xu KS;Li HL
目的：研究缺血再灌注损伤对大鼠原位肝移植模型肠组织钙-三磷酸腺苷酶活性的影响，探讨低氧预适应(HP)是否诱导缺氧诱导因子-1α对大鼠肠组织缺血再灌注损伤的保护作用。大鼠接受非致死性低氧预适应治疗，诱导缺氧诱导因子-1α表达。采用自体原位肝移植模型模拟肠组织I/R损伤。观察术后48h内小肠组织的超微结构变化、Ca2+-ATPase活性、细胞凋亡和炎症反应。低氧90min组大鼠术后12h肠组织中缺氧诱导因子-1α的表达显著高于非HP组(HP vs AT，P=0.0177)。对肠黏膜细胞进行病理分析，HP组的细胞比AT组的细胞健康。AT组术后小肠细胞钙-ATPase活性明显低于AT组，HP组术后6h恢复快于AT组(HP vs AT，P=0.0106)。术后12h，HP组bcl2表达明显高于AT组(P=0.0010)。炎症因子NO、超氧化物歧化酶、IL-6、肿瘤坏死因子-α在HP组的表达明显低于AT组。缺氧诱导的低氧诱导的α对肠粘膜细胞的线粒体损伤具有保护作用。HP可提高小鼠小肠粘膜细胞耐缺氧能力，提高细胞内Ca~(2+)-ATPase活性，从而减轻肠细胞的凋亡和病理损伤。幽门螺杆菌是促进移植物术后早期肠功能恢复的有效方法。
To investigate the effect of ischaemia and reperfusion (I/R) injury on the Ca2+-ATPase activation in the intestinal tissue of a rat autologous orthotopic liver transplantation model and to determine if hypoxia preconditioning (HP) therapy induces HIF-1α to protect rat intestinal tissue against I/R injury. Rats received non-lethal hypoxic preconditioning therapy to induce HIF-1α expression. We used an autologous orthotopic liver transplantation model to imitate the I/R injury in intestinal tissue. Then, we detected the microstructure changes in small intestinal tissues, Ca2+-ATPase activity, apoptosis, and inflammation within 48 h postoperatively. HIF-1α expression was significantly increased in intestinal tissue at 12 h postoperatively in rats that were exposed to a hypoxic environment for 90 min compared with a non-HP group (HP vs AT, P = 0.0177). Pathological analysis was performed on the intestinal mucosa cells, and the cells in the HP group appeared healthier than the cells in the AT group. The Ca2+-ATPase activity in the small intestinal cells in the AT group was significantly lower after the operation, and the Ca2+-ATPase activity in the HP group recovered faster than that in the AT group at 6 h postoperatively (HP vs AT, P = 0.0106). BCL-2 expression in the HP group was significantly higher than that in the AT group at 12 h postoperatively (HP vs AT P = 0.0010). The expression of the inflammatory factors NO, SOD, IL-6, and TNF-α was significantly lower in the HP group than in the AT group. Hypoxia-induced HIF-1α could protect intestinal mucosal cells against mitochondrial damage after I/R injury. HP could improve hypoxia tolerance in small intestinal mucosal cells and increase Ca2+-ATPase activity to reduce the apoptosis of and pathological damage to intestinal cells. HP could be a useful way to promote the earlier recovery of intestinal function after graft procedure.
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影响因子：
4.5
作者：
Schreiber, Rainer;Faria, Diana;Kunzelmann, Karl
通讯作者：
Kunzelmann, Karl
DOI：
10.1016/j.clinre.2014.12.012
发表时间：
2015-10-01
影响因子：
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作者：
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影响因子：
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作者：
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通讯作者：
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影响因子：
3.1
作者：
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通讯作者：
Kone, BC
影响因子：
21.3
作者：
Saito, M;Korsmeyer, SJ;Schlesinger, PH
通讯作者：
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