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胃扩张预处理对大鼠肾缺血/再灌注损伤的保护作用

Protective Effect of Gastric Distension Preconditioning on Renal Ischemia/Reperfusion Injury in Rats.

作者信息

Malek M, Maleki M

机构信息

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Iran.

Department of Physiology, School of Medicine, Ilam University of Medical Sciences, Ilam, Iran.

出版信息

Indian J Nephrol. 2018 Mar-Apr;28(2):113-118. doi: 10.4103/ijn.IJN_342_16.

DOI:10.4103/ijn.IJN_342_16
PMID:29861561
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5952449/
Abstract

The stomach mechanoreceptors can be stimulated by gastric distension (GD) and through afferent vagal nerve, increased activity of the renal sympathetic pathways. Because renal sympathectomy can abolish the protective effect of ischemic preconditioning, it seems that GD preconditioning can be effective in renal ischemia/reperfusion (I/R) injury. Gastric inflate (8 ml of 37°C water for 20 min) by a latex balloon inserted into the stomach through the fundus; I/R group was subjected to 45 min of bilateral ischemia and 24 h of reperfusion. GD preconditioning decreases blood urea nitrogen, creatinine, kidney damage score, and alkaline phosphatase levels compared to the sham GD group ( < 0.05). GD preconditioning may protect renal I/R injury through anti-inflammatory activity, but this efficacy requires extensive studies on the methods and mechanisms.

摘要

胃机械感受器可被胃扩张(GD)刺激,并通过迷走神经传入,增加肾交感神经通路的活性。由于肾交感神经切除术可消除缺血预处理的保护作用,因此GD预处理似乎对肾缺血/再灌注(I/R)损伤有效。通过经胃底插入胃内的乳胶气球向胃内注入(37℃水8ml,持续20分钟);I/R组经历45分钟的双侧缺血和24小时的再灌注。与假GD组相比,GD预处理可降低血尿素氮、肌酐、肾损伤评分和碱性磷酸酶水平(<0.05)。GD预处理可能通过抗炎活性保护肾I/R损伤,但这种疗效需要对方法和机制进行广泛研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/15c2514656e7/IJN-28-113-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/5257815bdcaf/IJN-28-113-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/6f5a4b6010e7/IJN-28-113-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/5468057dd0ef/IJN-28-113-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/5ba2994cd146/IJN-28-113-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/173d61bf5334/IJN-28-113-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/15c2514656e7/IJN-28-113-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/5257815bdcaf/IJN-28-113-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/6f5a4b6010e7/IJN-28-113-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/5468057dd0ef/IJN-28-113-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/5ba2994cd146/IJN-28-113-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/91e7/5952449/15c2514656e7/IJN-28-113-g006.jpg

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本文引用的文献

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World J Gastroenterol. 2015 Jul 14;21(26):8081-8. doi: 10.3748/wjg.v21.i26.8081.
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Hypoxic Conditioning as a New Therapeutic Modality.低氧适应作为一种新的治疗方式。
Front Pediatr. 2015 Jun 22;3:58. doi: 10.3389/fped.2015.00058. eCollection 2015.
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Renal ischemia/reperfusion injury; from pathophysiology to treatment.肾缺血/再灌注损伤:从病理生理学到治疗
J Renal Inj Prev. 2015 Jun 1;4(2):20-7. doi: 10.12861/jrip.2015.06. eCollection 2015.
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Hyperoxia-induced preconditioning against renal ischemic injury is mediated by reactive oxygen species but not related to heat shock proteins 70 and 32.高氧诱导的肾缺血损伤预处理由活性氧介导,但与热休克蛋白70和32无关。
Surgery. 2015 Jun;157(6):1014-22. doi: 10.1016/j.surg.2015.01.025. Epub 2015 Apr 3.
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The preventive effects of diminazene aceturate in renal ischemia/reperfusion injury in male and female rats.乙酰马啉对雄性和雌性大鼠肾缺血/再灌注损伤的预防作用。
Adv Prev Med. 2014;2014:740647. doi: 10.1155/2014/740647. Epub 2014 Nov 13.
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Heat shock preconditioning protects against ER stress-induced apoptosis through the regulation of the BH3-only protein BIM.热休克预处理通过调控仅含BH3结构域的蛋白BIM来保护细胞免受内质网应激诱导的凋亡。
FEBS Open Bio. 2014 Sep 17;4:813-21. doi: 10.1016/j.fob.2014.09.004. eCollection 2014.
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