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作 者:陈洁[1,2] 曹建平[1] 崔海洋[1] 谢华[1]
机构地区:[1]沈阳军区总医院呼吸内科,110840 [2]大连医科大学研究生院,116000
出 处:《免疫学杂志》2016年第2期119-123,共5页Immunological Journal
基 金:辽宁省自然科学基金(201202244);2014年辽宁省临床能力建设项目(LNCCC-A06-2014)
摘 要:目的探讨蛋白酶激活受体2(PAR-2)在过敏性休克中的作用,为过敏性休克的治疗提供新的思路。方法昆明种雄性小鼠随机分成致敏组和对照组。致敏组小鼠于第1天腹腔注射致敏原,1周后加强注射1次,饲养3周后尾静脉注射致敏原诱发过敏性休克。对照组以同等量的PBS缓冲液代替。酶联免疫吸附法(ELISA)检测致敏组和对照组小鼠血清类胰蛋白酶及类糜蛋白酶含量;RT-PCR法检测血液中PAR-2相对表达量。结果成功建立过敏性休克小鼠模型,RT-PCR结果显示致敏后小鼠PAR-2 m RNA相对表达量为3.372±0.28,对照组为0.759±0.062,2组比较有显著性差异(P<0.01);ELISA结果显示致敏后小鼠血清类胰蛋白酶含量为72.378μg/L±8.018μg/L,正常对照组为20.265μg/L±1.953μg/L,2组比较有显著性差异(P<0.01),致敏后小鼠血清类糜蛋白酶含量(16.186μg/L±0.959μg/L)低于对照组(34.905μg/L±3.972μg/L),组间比较有显著性差异(P<0.01)。结论 PAR-2可能参与了过敏性休克的发病过程。This study performed to investigate the role of protease activated receptor 2 (PAR-2) in anaphylactic shock and provide new ideas for the treatment of anaphylactic shock. Kunming mice were randomly divided into two groups: sensitized and control groups. Mice in sensitized group were immunized by intraperitoneal injection of allergen at first day and then a booster injection was executed a week after. Anaphylactic shock was induced by tail vein injection three weeks later. Mice in control group were injected equal amount of PBS buffer. Enzyme-linked immunosorbent assay (ELISA) was used to detect the content of tryptase and chymase in mouse serum; RT-PCR was used to detect the relative expression of PAR-2 mRNA. The results indicted that the relative expression of PAR-2 mRNA in sensitized group (3.372±0.28) increased significantly as compared with the control group (0.759±0.062)(P〈0.01). ELISA results indicated that the expression of tryptase in sensitized group (72.378 μg/ L±8.018 μg/L) increased significantly as compared with the control group (20.265 μg/L±1.953 μg/L) (P〈0.01), while the expression of ehymase in sensitized group (16.186μg/L±0.959 μg/L) decreased significantly as compared with control group (34.905μg/L ±3.972μg/L) (P〈0.01). Taken together, we can draw a conclusion that PAR-2 may involve in the pathogenesis of anaphylactic shock.
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