Protein Kinases C Changes in Rat Alveolar Macrophages during Sepsis

在敗血症時鼠肺泡巨噬細胞蛋白激醇C的改變

王文育(Wen-Yu Wang) ； 王東衡(Tung-Heng Wang) ； 王傳生(Chuan-Sheng Wang) ； 蔡忠榮(Jong-Rung Tsai) ； 許超群(Chau-Chyun Sheu) ； 洪仁宇(Jen-Yu Hung) ； 許德宏(Te-Hung Hsu) ； 黃明賢(Ming-Shyan Huang)

《胸腔醫學》 20卷5期 (2005/10) Pp. 354-361

https://doi.org/10.29806/TM.200510.0001

摘要

敗血症和急性呼吸窘迫症候群(ARDS)是住院病人致病及致死的主要原因。伴隨敗血症的許多生理失調是由於發炎介質的作用，然而，肺泡巨噬細胞在敗血症時發生ARDS的病理基因角色仍然未明。我們研究鼠肺泡巨噬細胞在敗血症時之蛋白激酶C(PKC)及鈣／調鈣蛋白依賴性蛋白酶Ⅱ(CaM kinase Ⅱ)的活性改變。雄性Sprague-Dawley鼠經由假性剖腹手術(sham)和盲腸結紮及穿刺(CLP)來誘發敗血症，肺泡巨噬細胞在CLP後第九小時（敗血症早期）和第十八小時（敗血症晚期）經由支氣管肺泡灌洗液(BALF)分離出來並培養兩小時，然後，分析肺泡巨噬細胞之細胞質成分中PKC和CaM kinaseⅡ的活性。CaM kinaseⅡ的活性從敗血症早期至晚期逐漸增加，在敗血症晚期PKC活性增加184%而CaM kinaseⅡ活性增加73.5%。我們的研究指出PKC及CaM kinaseⅡ的改變參與了敗血症時ARDS的發生。

關鍵字

肺泡巨噬細胞 ； 蛋白激酶C ； 敗血症

並列摘要

Sepsis and acute respiratory distress syndrome (ARDS) are major causes of morbidity and mortality in hospitalized patients. Many of the physiological derangements associated with sepsis are caused by inflammatory mediators. The pathogenetic roles of alveolar macrophages in the development of sepsis-induced ARDS are not fully clear. We therefore studies the protein kinase C (PKC) and Ca(superscript 2+)/calmodulin-dependent protein kinase Ⅱ (CaM kinase Ⅱ) activity of rat alveolar macrophages during sepsis. Sepsis was induced by cecal ligation and puncture (CLP) in male Sprague-Dawley rats. The control animals received only laparotomy without CLP. Alveolar macrophages were isolated 9 hr (early state of sepsis) and 18 hr (late state of sepsis) after CLP from bronchoalveolar lavage fluid (BALF), and cultured for 2 hours. The cytosolic fraction of the alveolar macrophages was assayed for PKC and CaM kinase Ⅱ activity. This activity increased progressively during early and late sepsis. PKC activity increased by 184% (P＜0.01) and CaM kinase Ⅱ activity was stimulated by 73.5% (P＜0.01) during the late sepsis. Our results indicate that the modification of PKC and CaM kinase Ⅱ may be involved in the development of ARDS during sepsis.

並列關鍵字

alveolar macrophage ； protein kinase C ； sepsis