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Blockade of high mobility group box-1 protein attenuates experimental severe acute pancreatitis

查看全文 作  者:Hidehiro [1]Sawa;Takashi [1]Ueda;Yoshifumi [2]Takeyama;Takeo [1]Yasuda;Makoto [1]Shinzeki;Takahiro [1]Nakajima;Yoshikazu [1]Kuroda 高影响力作者 机构地区:[1]Department of Gastroenterological Surgery, Kobe University Graduate School of Medical Sciences, Kobe 650-0017, Japan;[2]Department of Surgery, Kinki University School of Medicine, Osaka-sayama 589-8511, Japan高影响力机构 出  处:《World Journal of Gastroenterology》索引2006年第12卷第47期,共5页高影响力期刊 基  金:Supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Science, Sports and Culture of Japan and from the Ministry of Health, Labor and Welfare of Japan 摘  要:AIM: To examine the effects of anti-high mobility group box 1 (HMGB1) neutralizing antibody in experimental se-vere acute pancreatitis (SAP).METHODS: SAP was induced by creating closed duode-nal loop in C3H/HeN mice. SAP was induced immediately after intraperitoneal injection of anti-HMGB1 neutralizing antibody (200 μg). Severity of pancreatitis, organ injury (liver, kidney and lung), and bacterial translocation to pancreas was examined 12 h after induction of SAP.RESULTS: Anti-HMGB1 neutralizing antibody significant-ly improved the elevation of the serum amylase level and the histological alterations of pancreas and lung in SAP. Anti-HMGB1 antibody also significantly ameliorated the elevations of serum alanine aminotransferase and cre-atinine in SAP. However, anti-HMGB1 antibody worsened the bacterial translocation to pancreas.CONCLUSION: Blockade of HMGB1 attenuated the development of SAP and associated organ dysfunction, suggesting that HMGB1 may act as a key mediator for inflammatory response and organ injury in SAP. 关 键 词:急性胰腺炎 十二指肠 细菌易位 丙胺酸
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