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机构地区:[1]武汉大学人民医院老年病科,湖北武汉430060 [2]武汉大学人民医院检验科,湖北武汉430060 [3]武汉大学人民医院心内科,湖北武汉430060
出 处:《武汉大学学报(医学版)》2016年第2期191-194,199,共5页Medical Journal of Wuhan University
基 金:国家自然科学基金青年基金资助项目(编号:81200058)
摘 要:目的:探讨CXCR3在内毒素脂多糖(LPS)所致小鼠急性肺损伤(ALI)发病机制中的作用及与白细胞介素-10(IL-10)的关系。方法:将24只雄性C57BL/6小鼠分为正常组、LPS 2h组及LPS 12h组。HE染色观察肺组织病理改变;流式细胞术检测肺泡灌洗液(BALF)和肺组织CD8+T细胞及CD4+T细胞百分比;酶联免疫吸附试验及实时荧光定量PCR分别检测BALF和肺组织中IL-10和CXCR3的表达。结果:LPS 12h组BALF和肺组织炎症细胞数及CXCR3的表达均较正常组及LPS 2h组增多(P<0.05);IL-10的表达较正常组及LPS 2h组降低(P<0.05),且与CXCR3的表达及CD8+T细胞数呈负相关(P均<0.05)。结论:CXCR3可参与急性肺损伤炎症的发生与发展,且与IL-10的表达呈负相关。重建CXCR3及IL-10的平衡可能会成为治疗ALI的新目标。Objective: To investigate the roles of CXCR3 in the pathogenesis of acute lung injury (ALI) induced by lipopolysaceharide (LPS) and its relationship to Interleukin 10 (IL-10). Methods: Twenty-four healthy male C57BL/6 mice were divided into control group, LPS 2 h group and LPS 12 h group. The lung histopathology changes were observed by HE staining. The percent- age of CD4+ T cells and CD8+ T cells in bronchoalveolar lavage fluids (BALF) and lungs were ex- amined by FCM. Expression of IL-10 and CXCR3 in BALF and lung tissue were detected by ELISA and real-time quantitative PCR. Results: Compared with the LPS 2 h group and normal group mice, LPS 12 h group mice showed higher LPS-induced lung inflammation as evidenced by more infiltration of inflammatory cells in airways and lung tissue, higher levels of CXCR3, and lower levels of IL-10(P〈0.05). The level of CXCR3 showed a negative correlation with the level of IL-10, and the percentage of CD8+T cells from BALF and lungs negatively correlated with the level of IL-10. Conclusion: The findings show that CXCR3 participate in the occurrence and de- velopment of ALI, and correlates positively to the level of IL-10. Rebuilding the balance between CXCR3 and IL-10 may be a novel therapeutic target for ALI treatment.
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