본문 바로가기
KERD
논문KCI 미등재

내독소로 유도된 급성 폐 손상에서 게르마늄의 투여로 인한호중구 세포사의 증가

Germanium Increases Alveolar Macrophage Engulfment ofApoptotic Neutrophils in Acute Lung Injury Induced by Endotoxin

2

조회

0

다운로드

3

인용

0

참고문헌

주제분류자연과학일반

초록

호중구는 다양한 원인에 의해서 발생되는 급성 폐 손상의 발병기전에 중요한 역할을 담당한다. 폐 손 상 시 순환계로부터 유입된 호중구들에 대한 폐포강 대식세포의탐식작용이 증가될 경우 손상기전에 미치는 영향을 알아보기 위해 내독소를 흰쥐의 기관지 내로 분무하고 유기게르마늄을 복강으로 투여하였다.실험 결과 내독소 투여 5시간 후 체중당 폐 무게와 폐세척액 내 단백질 함량은 유의하게 (p0.001) 증가되었으나, 게르마늄 병행 투여로 폐 무게와 단백질 함량은 현저하게 (p0.001, p0.01) 감소되었다. 내독소 투여군은 폐 손상과 함께 폐포강 내 호중구는 유의하게 (p0.05) 증가되었으나, 게르마늄의 투여로 감소되었고 폐포강 내탐식된 호중구의 비율은 증가되었다. 이와 같은 결과들을 볼 때, 유기 게르마늄은 내독소증 에 의한 급성 폐 손상에서 폐포강 대식세포들의 호중구 탐식작용을 증가시켜 폐 손상을 감소시킬 수 있는 것으로 나타났다.

Abstract

Neutrophils that influx into the alveolar spaces from circulatory bloods play a important role in pathogenesisof acute lung injury. During the acute inflammatory phase, in order to investigate the acceleration ofmacrophage phagocytosis to the neutrophils is able to reduce the neutrophil-derived acute lung injury,endotoxemia was induced by insufflation of lipopolysaccharide intratracheally and organic germanium wasinjected intraperitoneally after endotoxin treatment.At 5 h after endotoxin treatment, lung weight and BAL protein concentration are significantly increased(p0.001) compared to sham, and that was remarkedly decreased (p0.001, p0.01) by injection ofgermanium. In addition germanium treatment resulted to decreased the number of alveolar PMNs and toincrease the percentage of engulfed neutrophils by alveolar macrophages.These observations indicate that organic germanium may have a role of reduction to neutrophil-derivedacute lung injury in endotoxemia.

참고문헌 (16)

  1. "Induction of interferone and activation of NK cells andmacrophages in mice by oral administration of Ge-132", pp.65~74 (1985)
  2. "elimination of interfering substance.Anal Biochem 102", pp.1152~1160 (1989), Protein measurement usingbicinconinic acid
  3. "Macrophage engulfment of apoptoticneutrophils contributes to the resolution of acute pulmonaryinflammation in vivo. Am J Respir Cell Mol Biol12" (1995)
  4. "TNFalpha-induced suppression of PMN apoptosis ismediated through interleukin-8 production. Shock 14", 14(3), pp.284~289 (2000)
  5. "Role of NF-kB in endotoxemia-induced alterationof lung neutrophil apoptosis. J Immunol 167", 167(12), pp.7044~7051 (2001)
  6. "Platelet activating-factor induces lung inflammation and leak in rats hydrogenperoxide production along neutrophil-lung endothelialcell interfaces. J Lab Clin Med 140", pp.312~319 (2002)
  7. "Mepacrine decreases lung leak in rats giveninterleukin-1 intratracheally. Am J Respir Crit Care Med155", pp.1624~1628 (1997)
  8. "Effectof the inhibition of phospholipase A2 in generation of freeradicals in intestinal ischemia", reperfusion induced acutelung injury. Kor J Physiol Pharmacol 3, 1999., 263~273
  9. "Modulation of neutrophil apoptosisby glanulocyte colony-stimulating factor and glanulocyte", macrophage colony-stimulating factor during thecourse of acute respiratory distress syndrome. Crit CareMed 28, 2000., pp.28(1), ~
  10. "Alveolarmacrophages that phagocytose apoptotic neutrophils producehepatocyte growth factor during bacterial pneumoniain mice. Am J Respir Cell Mol Biol 24", pp.608~615 (2001)
  11. "Phagocytosis of senescentneutrophils by human monocyte-derived macrophagesand rabbit inflammatory macrophages. J Exp Med156" (1982)
  12. "Neutrophilapoptosis in the lung after hemorrhage or endotoxemia apoptosis and migration are independent of IL-1β. ClinImmunol 91", 219 (1999)
  13. "Macrophage phagocytosis of aging neutrophilsin inflammation programmed cell death in the neutrophilleads to its recognition by macrophages. J Clin Invest 83" (1989)
  14. "Macrophage myeloperoxidase regulation byglanulocyte macrophage colony-stimulating factor in humanatherosclerosis and implications in acute coronarysymdromes. Am J Pathol 158", 158(3), pp.879~891 (2001)
  15. "Cooperation of lymphokine and macrophages in expression of antitumoractivity of carboxyethylgermanium", pp.177~132 182 (1986)
  16. "Activation of the Fas receptoron lung eosinophils leads to apoptosis and the resolution ofeosinophilic inflammation of the airways. J Clin Invest 96", 2924 (1995)

관련 논문AI추천

이 간행물의 다른 논문 (11건)