急性腎臟傷害下CCL5調節急性肺傷害的角色

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題名:	急性腎臟傷害下CCL5調節急性肺傷害的角色 CCL5 mediates acute lung injury following acute kidney injury
作者:	蔡宗訓;Tsai, Tsung-Hsun
貢獻者:	醫學研究所碩士班
關鍵詞:	急性腎傷害;急性肺傷害;CCL5;RANTES;acute kidney injury;acute lung injury
日期:	2012-08-03
上傳時間:	2012-08-31 16:38:29 (UTC+8)
出版者:	中國醫藥大學
摘要:	儘管現在洗腎技術和設備的進步，急性腎臟衰竭患者合併多重器官衰竭的存活率仍是偏低。在休克或血管損傷情形下已被發現有肺部傷害的產生，然而在單純的腎臟缺血和再灌流情形下的效應則仍未明確。就目前研究實驗已發現細胞激素(cytokine)和趨化細胞激素(chemokine)在急性腎臟受傷扮演重要角色，而CCL5 (又稱RANTES) 為C-C趨化細胞激素的一員，在急性腎臟缺血再灌注時會產生，並導致後續組織細胞傷害的情形。因此，在本研究針對CCL5在急性腎臟缺血再灌流的情形下對肺部傷害的調節作用加以探討。我們選擇野生型C57BL/6 和CCL5-/-8至10週，體重20-25公克的雄性小鼠進行研究。實驗中將小鼠予以雙側腎臟血管夾住60分鐘後給予再灌流，並分別於6小時和24小時將小鼠加以解剖。血清在每個時間點經由心臟穿刺採血加以收集檢測腎功能BUN數值變化。肺臟傷害則於每個時間點取肺部組織檢體，利用組織染色、免疫螢光學檢測來加以評估。從肺部的組織染色發現CCL5-/-的小鼠在間質組織水腫，肺泡出血和組織充血的情形有明顯改善。肺部嗜中性白血球數量在6小時有顯著增加且在24小時後減少。肺部MPO活性和IL-6的表現也在CCL5-/-的小鼠在免疫螢光學染色亦有相當程度改善。從以上實驗結果發現，在急性腎臟缺血再灌流的情形下，CCL5在後續急性肺傷害扮演調解角色。並藉由這結果來加以明瞭急性腎傷害下導致呼吸功能受損的影響機轉。 Although the advances of dialysis technology and equipment, survival rate with acute renal failure when complicated with multiorgan failure is still low. In the case of visceral injury or shock has been found to induce lung injury, but the influences of acute renal ischemia reperfusion injury (IRI) on the lungs are not yet clear. The present experiments have found that the cytokines and chemokines play an important roles in lung injury following acute kidney injury. CCL5(also known as RANTES), a member of C-C chemokine, will produce and lead to subsequent tissue injury situations in acute renal ischemia reperfusion injury. There, we hypothesized that in acute renal ischemia reperfusion injury may result in acute lung injury and that CCL5 is an important mediators in this reaction. We choice 8-10 weeks, weight 20-25 g wide type C57BL/6 and CCL5-/-, male mice to study. The mice underwent the clamp of bilateral renal vessels for 60 minutes, followed by reperfusion, respectively, in 6 hours and 24 hours, the mice were to be scarified. Serum blood was collected to detect renal BUN level change at each time pint via cardiac puncture. Lung injury was assessed by histology, immunohistochemistry stain at each time point after reperfusion. After acute renal ischemia reperfusion injury, the CCL5-/- mice in the interstitial tissue edema, alveolar hemorrhage and tissue congestion from the pulmonary histology showed the significant improvement. The neutrophil counts in lung also showed significant increase at 6 hours and decrease at 24 hours. In the immunofluorescence studies, lung MPO activity and IL-6 also increase during renal ischemia reperfusion injury in wild type and attenuate in CCL5-/- mice at each time point. From the above experimental results, acute lung injury develops after acute renal ischemia reperfusion injury, and CCL5 play a mediation role in this pathway. These results will allow us to understand the mechanism of the impact of impoaired respiratory function associate with acute kidney injury.
顯示於類別:	[醫學研究所] 博碩士論文

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