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Ischemia-Reperfusion Injury : Pathophysiology and Clinical Implications.缺血再灌注损伤:病理生理学与临床意义
Eur J Trauma Emerg Surg. 2007 Dec;33(6):600-12. doi: 10.1007/s00068-007-7152-z. Epub 2007 Nov 20.
2
Postconditioning of the lower limb--protection against the reperfusion syndrome.下肢预处理——防止再灌注综合征。
J Surg Res. 2011 Jul;169(1):139-47. doi: 10.1016/j.jss.2009.10.014. Epub 2009 Nov 3.
3
Hind limb ischemic preconditioning induces an anti-inflammatory response by remote organs in rats.下肢缺血预处理通过远程器官诱导大鼠产生抗炎反应。
Braz J Med Biol Res. 2009 Oct;42(10):921-9. doi: 10.1590/s0100-879x2009005000025. Epub 2009 Sep 11.
4
Metabolic consequences of acute limb ischemia and their clinical implications.急性肢体缺血的代谢后果及其临床意义。
Semin Vasc Surg. 2009 Mar;22(1):29-33. doi: 10.1053/j.semvascsurg.2009.01.001.
5
[Hypoxia induced HIF-1 accumulation and VEGF expression in gastric epithelial mucosa cell: involvement of ERK1/2 and PI3K/Akt].[缺氧诱导胃上皮黏膜细胞中HIF-1积累及VEGF表达:ERK1/2和PI3K/Akt的参与]
Mol Biol (Mosk). 2008 May-Jun;42(3):459-69.
6
Reactive oxygen species regulate hypoxia-inducible factor 1alpha differentially in cancer and ischemia.活性氧在癌症和缺血中对缺氧诱导因子1α的调节作用不同。
Mol Cell Biol. 2008 Aug;28(16):5106-19. doi: 10.1128/MCB.00060-08. Epub 2008 Jun 16.
7
Oxidative stress and ischemia-reperfusion injury in gastrointestinal tract and antioxidant, protective agents.氧化应激与胃肠道缺血再灌注损伤及抗氧化、保护剂。
J Clin Biochem Nutr. 2007 Jan;40(1):1-12. doi: 10.3164/jcbn.40.1.
8
Limb remote-preconditioning protects against focal ischemia in rats and contradicts the dogma of therapeutic time windows for preconditioning.肢体远程预处理可保护大鼠免受局灶性缺血损伤,并与预处理治疗时间窗的教条相矛盾。
Neuroscience. 2008 Feb 19;151(4):1099-103. doi: 10.1016/j.neuroscience.2007.11.056. Epub 2007 Dec 15.
9
Essential role of extracellular SOD in reparative neovascularization induced by hindlimb ischemia.细胞外超氧化物歧化酶在后肢缺血诱导的修复性新生血管形成中的重要作用。
Circ Res. 2007 Aug 17;101(4):409-19. doi: 10.1161/CIRCRESAHA.107.153791. Epub 2007 Jun 29.
10
Extracellular signal-regulated kinase pathways may mediate the protective effect of electrical stimulation of the paraventricular nucleus against ischaemia-reperfusion injury of the gastric mucosa.细胞外信号调节激酶通路可能介导室旁核电刺激对胃黏膜缺血-再灌注损伤的保护作用。
Clin Exp Pharmacol Physiol. 2007 Aug;34(8):742-52. doi: 10.1111/j.1440-1681.2007.04652.x.

胃缺血时的氧化应激和缺氧诱导因子 1α 表达。

Oxidative stress and hypoxia-induced factor 1α expression in gastric ischemia.

机构信息

Department of Anesthesiology, The First Hospital of Lanzhou University, Lanzhou 73000, Gansu Province, China.

出版信息

World J Gastroenterol. 2011 Apr 14;17(14):1915-22. doi: 10.3748/wjg.v17.i14.1915.

DOI:10.3748/wjg.v17.i14.1915
PMID:21528068
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3080729/
Abstract

AIM

To investigate the relation of reactive oxygen species (ROS) to hypoxia induced factor 1α (HIF-1α) in gastric ischemia.

METHODS

The animal model of gastric ischemia reperfusion was established by placing an elastic rubber band on the proximal part of the bilateral lower limb for ligature for 3 h and reperfusion for 0, 1, 3, 6, 12 or 24 h. Ischemic post-conditioning, three cycles of 30-s reperfusion and 30-s femoral aortic reocclusion were conducted before reperfusion. Histological and immunohistochemical methods were used to assess the gastric oxidative damage and the expression of HIF1-α in gastric ischemia. The malondialdehyde (MDA) content and superoxide dismutase (SOD), xanthine oxidase (XOD) and myeloperoxidase (MPO) activities were determined by colorimetric assays.

RESULTS

Ischemic post-conditioning can reduce post-ischemic oxidative stress and the expression of HIF-1α of gastric tissue resulting from limb ischemia reperfusion injury. MDA, SOD, XOD and MPO were regarded as indexes for mucosal injuries from ROS, and ROS was found to affect the expression of HIF-1α under gastric ischemic conditions.

CONCLUSION

ROS affects HIF-1α expression under gastric ischemic conditions induced by limb ischemia reperfusion injury. Therefore, ROS can regulate HIF-1α expression in gastric ischemia.

摘要

目的

探讨活性氧(ROS)与胃缺血缺氧诱导因子 1α(HIF-1α)的关系。

方法

通过在双侧下肢近端放置弹性橡皮筋结扎 3 h 并再灌注 0、1、3、6、12 或 24 h 来建立胃缺血再灌注动物模型。在再灌注前进行缺血后处理,即 3 个循环的 30 s 再灌注和 30 s 股动脉再闭塞。采用组织学和免疫组织化学方法评估胃氧化损伤和胃缺血中 HIF1-α的表达。通过比色法测定丙二醛(MDA)含量和超氧化物歧化酶(SOD)、黄嘌呤氧化酶(XOD)和髓过氧化物酶(MPO)活性。

结果

肢体缺血再灌注损伤后,缺血后处理可减轻缺血后氧化应激和胃组织 HIF-1α的表达。MDA、SOD、XOD 和 MPO 被视为 ROS 引起的黏膜损伤指标,并且在胃缺血条件下 ROS 被发现影响 HIF-1α的表达。

结论

ROS 影响肢体缺血再灌注损伤诱导的胃缺血条件下 HIF-1α的表达。因此,ROS 可以调节胃缺血时 HIF-1α的表达。