博文
氢气治疗小肠缺血再灌注损伤后细胞凋亡
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终于等到全文和正式页码
The Effects of Hydrogen-Rich Saline on the Contractile and Structural Changes of.pdf
Journal of Surgical Research, Volume 167, Issue 2, 15 May 2011, Pages 316-322
Han Chen, Yan Ping Sun, Ping Fang Hu, Wen Wu Liu, Hong Gang Xiang, Yang Li, Rong Lin Yan, Ning Su, Can Ping Ruan, Xue Jun Sun, Qiang Wang
关于小肠缺血再灌注，我们已经发表了3篇论著，这是我们与长征医院普外科王主任合作的研究，因为以前已经发表了2篇同一模型的论文，本研究尽管在研究深度上推进了一步，但发表仍是比较慢了一些。该论著是该领域的第22篇论著。
从07年的第一篇，到现在的22篇，平均每月1篇，估计8月仍应该有2篇发表。
Methods. Intestinal I/R injury was induced in Sprague-Dawley rats using bulldog clamps in superior mesenteric artery by 45 min ischemia followed by 1 h reperfusion. Rats were divided randomly into four groups: sham-operated, I/R, I/R plus saline treatment, and I/R plus hydrogen-rich saline treatment groups. Hydrogen-rich saline ( > 0.6 mM, 6 ml/kg) or saline (6 ml/kg) was administered respectively via tail vein in 30 min prior to reperfusion. Following reperfusion, segments of terminal jejunum were rapidly taken and transferred into isolated organ bath and responses to KCl were recorded. Samples of terminal jejunum were also taken for measuring malondialdehyde and myeloperoxidase. Apoptosis in intestinal epithelium was determined with terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling technique (TUNEL). Expression and distribution of proliferating cell nuclear antigen (PCNA) were detected with immunohistochemistry.
Results. Hydrogen-rich saline treatment significantly attenuated the severity of intestinal I/R injury with inhibiting I/R-induced apoptosis and promoting enterocytes proliferation. Moreover, Hydrogen-rich saline treatment significantly limited the neutrophil infiltration, lipid oxidation and ameliorated the decreased contractility response to KCl in the intestine subjected to I/R.
Conclusions. These results suggest that hydrogen treatment has a protective effect against intestinal contractile dysfunction and damage induced by intestinal I/R. This protective effect is possibly due to its ability to inhibit I/R-induced oxidative stress, apoptosis and to promote epithelial cell proliferation.
Keywords: Hydrogen, Intestinal ischemia/reperfusion, Antioxidant, Oxidative stress, Contractility, Apoptosis
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