Summary： The role of protease activated receptor-2 （PAR-2） in the renal tubulointerstitial lesion induced by unilateral ureteral obstruction （UUO） was explored. Mice were sacrificed on the day 1, 3, 5, 7, 10, 14 ...Summary： The role of protease activated receptor-2 （PAR-2） in the renal tubulointerstitial lesion induced by unilateral ureteral obstruction （UUO） was explored. Mice were sacrificed on the day 1, 3, 5, 7, 10, 14 and 21 after UUO. The expression of PAR-2 mRNA and protein and a-smooth muscle actin （α-SMA） protein in tubuloin,terstitium was detected by RT-PCR and immunohistochemistry at each time point, respedtively. The results showed that the PAR-2 expression in renal tubulointerstitium was increased progressively starting from 24 h to the day 14 post-ligation, and it was significantly associated with the relative volume of interstitium and the positive area of α-SMA. PAR-2 was mainly expressed in renal tubule epithelial cells, especially in proximal tubular cells. It also located in renal capillary ansa, interstitial infiltrate cells and fibroblasts. It was concluded that PAR-2 was active in interstitial and tubular cells in the early phase of fibrotic process and played an important role in mediating the tubulointerstitial lesion after UUO.展开更多
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。...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。展开更多
文摘Summary： The role of protease activated receptor-2 （PAR-2） in the renal tubulointerstitial lesion induced by unilateral ureteral obstruction （UUO） was explored. Mice were sacrificed on the day 1, 3, 5, 7, 10, 14 and 21 after UUO. The expression of PAR-2 mRNA and protein and a-smooth muscle actin （α-SMA） protein in tubuloin,terstitium was detected by RT-PCR and immunohistochemistry at each time point, respedtively. The results showed that the PAR-2 expression in renal tubulointerstitium was increased progressively starting from 24 h to the day 14 post-ligation, and it was significantly associated with the relative volume of interstitium and the positive area of α-SMA. PAR-2 was mainly expressed in renal tubule epithelial cells, especially in proximal tubular cells. It also located in renal capillary ansa, interstitial infiltrate cells and fibroblasts. It was concluded that PAR-2 was active in interstitial and tubular cells in the early phase of fibrotic process and played an important role in mediating the tubulointerstitial lesion after UUO.
文摘目的:探究蛋白酶激活受体2(protease-activated receptor 2,PAR2)对人内皮祖细胞(endothelial progenitor cell,EPC)功能的影响。方法:EPC予以PAR2天然激动剂类胰蛋白酶、合成激动剂SLIGKV-NH2、合成抑制剂FSLLRY-NH2处理,EdU、Transwell实验观察EPC增殖、迁移,实时定量PCR、ELISA分析检测相关细胞因子及受体表达,免疫印迹法评估Ras同源家族成员A(Ras homolog family member A,RhoA)水平;同时给予RhoA特异性抑制剂Y-27632,观察PAR2活化效应可否被取消。结果:PAR2激动剂可剂量依赖性抑制EPC增殖及迁移(P<0.05),下调血管内皮生长因子A、血管内皮生长因子受体2、基质细胞衍生因子1及趋化性细胞因子受体4等表达(P<0.05),该效应可被PAR2抑制剂取消;活化PAR2可显著上调EPC RhoA表达(P<0.05),抑制PAR2活性可取消该效应;Y-27632可逆转PAR2激动剂导致的EPC细胞增殖、迁移抑制(P<0.05)。结论:PAR2经RhoA信号抑制EPC增殖、迁移功能,是极具潜力的内皮再生与血管生成调控靶点。
文摘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。
