低氘氫水實驗室

關於小腸缺血再灌注，我們已經發表了3篇論著，這是我們與長征醫院普外科王主任合作的研究，因為以前已經發表了2篇同一模型的論文，本研究儘管在研究深度上推進了一步，但發表仍是比較慢了一些。該論著是該領域的第22篇論著。 從07年的第一篇，到現在的22篇，平均每月1篇，估計8月仍應該有2篇發表。     

Background. Hydrogen has been considered as a novel antioxidant that prevents injuries resulted from ischemia-reperfusion (I/R) injury in various tissues. The study was designed to determine the effect of hydrogen-rich saline on the smooth muscle contractile response to KCl, and on epithelial proliferation and apoptosis of intestine subjected to I/R. 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 m , 6 ml/kg) or saline M( 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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