来源
2008-3-17 17:06:11
Nature Medicine:日发现防止术后伤口粘连新方法
日本研究人员报告说，经研究发现，阻碍干扰素发挥作用可防止患者手术后伤口发生粘连。
日本共同社１７日报道说，日本兵库医科大学免疫学教授中西宪司等人发现，手术后，为了促进伤口血液凝固，人体内的干扰素会提升纤维状蛋白质的功能。这一过程虽然帮助伤口止血，但也可能诱使伤口部位出现粘连。干扰素是一类具有多种功能的活性蛋白质。
中西宪司等利用实验鼠确认，使用阻碍干扰素发挥作用的药剂，可防止术后发生伤口粘连。
外科手术后，伤口与周围组织的粘连问题是至今没有完全解决的医学难题。以腹部手术为例，不少患者会出现患部和周围组织粘合在一起，这往往导致剧烈的腹痛或者肠梗阻，而目前想彻底防止粘连还非常困难。
日本研究人员希望以这次的发现为基础，开发出防止伤口粘连的药物，以解除患者术后的苦恼。这一研究成果已发表在最新一期英国《自然·医学》杂志网络版上。
生物谷推荐原始出处：
Nature Medicine，doi:10.1038/nm1733，Hisashi Kosaka, Kenji Nakanishi
Interferon-
is a therapeutic target molecule for prevention of postoperative adhesion formation
Hisashi Kosaka1,5, Tomohiro Yoshimoto2,3,5, Takayuki Yoshimoto4, Jiro Fujimoto1 & Kenji Nakanishi2,3
Intestinal adhesions are bands of fibrous tissue that connect the loops of the intestine to each other, to other abdominal organs or to the abdominal wall1, 2, 3. Fibrous tissue formation is regulated by the balance between plasminogen activator inhibitor type 1 (PAI-1) and tissue-type plasminogen activator (tPA), which reciprocally regulate fibrin deposition. Several components of the inflammatory system, including cytokines4, chemokines, cell adhesion molecules and neuropeptide substance P, have been reported to participate in adhesion formation4, 5, 6, 7. We have used cecal cauterization to develop a unique experimental mouse model of intestinal adhesion. Mice developed severe intestinal adhesion after this treatment. Adhesion development depended upon the interferon-
(IFN-) and signal transducer and activator of transcription-1 (STAT1) system. Natural killer T (NKT) cell–deficient mice developed adhesion poorly, whereas they developed severe adhesion after reconstitution with NKT cells from wild-type mice, suggesting that NKT cell IFN- production is indispensable for adhesion formation. This response does not depend on STAT4, STAT6, interleukin-12 (IL-12), IL-18, tumor necrosis factor-
, Toll-like receptor 4 or myeloid differentiation factor-88–mediated signals. Wild-type mice increased the ratio of PAI-1 to tPA after cecal cauterization, whereas Ifng-/- or Stat1-/- mice did not, suggesting that IFN- has a crucial role in the differential regulation of PAI-1 and tPA. Additionally, hepatocyte growth factor, a potent mitogenic factor for hepatocytes8, 9, strongly inhibited intestinal adhesion by diminishing IFN- production, providing a potential new way to prevent postoperative adhesions.
(IFN-) and signal transducer and activator of transcription-1 (STAT1) system. Natural killer T (NKT) cell–deficient mice developed adhesion poorly, whereas they developed severe adhesion after reconstitution with NKT cells from wild-type mice, suggesting that NKT cell IFN- production is indispensable for adhesion formation. This response does not depend on STAT4, STAT6, interleukin-12 (IL-12), IL-18, tumor necrosis factor-, Toll-like receptor 4 or myeloid differentiation factor-88–mediated signals. Wild-type mice increased the ratio of PAI-1 to tPA after cecal cauterization, whereas Ifng-/- or Stat1-/- mice did not, suggesting that IFN- has a crucial role in the differential regulation of PAI-1 and tPA. Additionally, hepatocyte growth factor, a potent mitogenic factor for hepatocytes8, 9, strongly inhibited intestinal adhesion by diminishing IFN- production, providing a potential new way to prevent postoperative adhesions.- 众说风云 (已有0条评论)
