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血小板活化因子受体拮抗剂银杏内酯B抑制结肠炎相关癌症中的肿瘤发生和血管生成。

PAF receptor antagonist Ginkgolide B inhibits tumourigenesis and angiogenesis in colitis-associated cancer.

作者信息

Sun Lei, He Zhen, Ke Jia, Li Senmao, Wu Xianrui, Lian Lei, He Xiaowen, He Xiaosheng, Hu Jiancong, Zou Yifeng, Wu Xiaojian, Lan Ping

机构信息

Department of Colorectal Surgery, Sixth Affiliated Hospital, Sun Yat-Sen University Guangzhou City, Guangdong Province, P. R. China.

出版信息

Int J Clin Exp Pathol. 2015 Jan 1;8(1):432-40. eCollection 2015.

Abstract

Platelet activating factor (PAF), a potent pro-inflammatory phospholipid, has been found to trigger tumor growth and angiogenesis through its G-protein coupled receptor (PAFR). This study was aimed to investigate the potential role of PAF in azoxymethane (AOM)/dextran sulfate sodium (DSS) induced colitis-associated cancer (CAC), using PAFR antagonist Ginkgolide B (GKB). We found GKB up-regulated serum level of PAF-AH activity. As assessed by disease activity index (DAI), histological injury scores, leukocytes infiltration, and expression of pro-inflammatory cytokines, GKB ameliorated colonic inflammation and decreased tumor number and load in mice. GKB also decreased expression of vascular endothelial growth factor (VEGF) and microvessel density (MVD) in tumor. These results suggest that PAFR antagonist might be a potential therapeutic strategy for CAC.

摘要

血小板活化因子(PAF)是一种强效促炎磷脂,已发现它可通过其G蛋白偶联受体(PAFR)触发肿瘤生长和血管生成。本研究旨在使用PAFR拮抗剂银杏内酯B(GKB)研究PAF在氧化偶氮甲烷(AOM)/葡聚糖硫酸钠(DSS)诱导的结肠炎相关癌(CAC)中的潜在作用。我们发现GKB上调了血清PAF-AH活性水平。通过疾病活动指数(DAI)、组织学损伤评分、白细胞浸润和促炎细胞因子表达评估,GKB改善了小鼠的结肠炎症,并减少了肿瘤数量和负荷。GKB还降低了肿瘤中血管内皮生长因子(VEGF)的表达和微血管密度(MVD)。这些结果表明,PAFR拮抗剂可能是CAC的一种潜在治疗策略。

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