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Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway. 相似文献
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Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway. 相似文献
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Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway. 相似文献
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实验室检查提供了诊断疾病、监测病情、判断疗效及预后的依据。临床医师60%~70%的重要决策基于实验室检测结果,对实验室检测的质量与速度都有一定要求。随着技术的进步,检测质量已经有了很大的提高,临床对于提高检测速度越来越关注[1]。急诊检验处于医疗第一线,是抢救危重患者的重要环节,及时、准确地发出急诊检验报告尤为重要。急诊检验报告的及时性主要是用检验结果的回报告时间来评价的[2-3]。 相似文献
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【目的】 探讨抑制肾小管上皮间充质转化(EMT)过程中胚胎发育关键基因WT1和Pax2的表达对EMT的逆转作用。【方法】 采用RNAi技术分别抑制WT1和Pax2。分别构建pshRNA-WT1和pshRNA-Pax2表达载体,采用脂质体转染技术,使质粒瞬时转染NEK52E细胞后用10 ng/mL IL-1α刺激细胞,分别提取不同时间点细胞的RNA和蛋白质,采用RT-PCR和Western blot检测细胞WT1、Pax2、Snail、上皮细胞标志E-cadherin和间充质标志α-SMA的mRNA和蛋白质的表达,并观察NRK52E细胞的形态。【结果】构建的pshRNA-WT1和pshRNA-Pax2表达载体可在转染细胞内发挥RNAi作用抑制WT1和Pax2基因的表达,抑制率分别为80.4 %和82.7 %。分别抑制WT1和Pax2基因后EMT过程受阻,α-SMA和Snail的表达显著减少,E-cadherin的表达无显著性变化,细胞形态未发生明显的成纤维化样改变。【结论】 WT1和Pax2基因是EMT中的关键基因,分别抑制胚胎发育关键基因WT1和Pax2均可使EMT受阻。阻断WT1和Pax2的表达有望中止EMT及肾纤维化的发生。 相似文献
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目的:评估妊娠期糖尿病(GDM)患者的血小板(PLT)功能状态的变化情况及其临床意义。方法:选取2017年3月至2017年10月在广州市妇女儿童医疗中心产检的85例GDM患者为观察组,选取同期85例正常孕妇为对照组,收集其临床资料及乙二胺四乙酸(EDTA)抗凝全血,Sysmex XE–5000全自动血细胞分析仪进行血常规及网织血小板(ret–PLT)检测。结果:观察组患者PLT计数较对照组降低,而血小板平均体积(MPV)及未成熟血小板指数(IPF)、高荧光强度血小板分数(H–IPF%)等参数较对照组明显升高,差异具有统计学意义(P0.05)。结论:GDM患者PLT更新率升高,活化增强,检测PLT计数、IPF及H–IPF%等参数,可对GDM患者进行PLT功能评价,预测心血管并发症风险。 相似文献
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Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway. 相似文献
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Objective To investigate the effect of angiotensin (Ang) Ⅱ and its Janns-activated kinase-2 (JAK2) signal pathway in transdifferentiation of renal tubular cells under the challenge of acute ischemic reperfusion injury.Methods Models of acute ischemic reperfusion injury were established and the level of local Ang Ⅱ ,a key element of renin-angiotensin system (RAS),in kidney was measured using radioimmunity technique.The expression of α-smooth muscle actin (α-SMA),a phenotype of mesenchymal cells,was detected by RT-PCR and inununohistochemistry methods.Renal tubule cells ( NRK-52E) were cultured with various concentration of Ang Ⅱ ,followed by blocking of PD123319,Ang U receptor 2 antagonist,and AG490,an inhibitor of JAK2 signal pathway.Results Ang 0 of kidney tissue increased immediately after acute ischemic-reperfusion injury,in time dependent fashion.Expression of α-SMA in renal tubule cells was found at 48 hours after ischemic-reperfusion injury and in NRK-52E cells treated by high concentration of Ang Ⅱ and was dose and time dependent.The peak of α-SMA expression was seen after 30 minute treatment at the dose of 10-9'mol/L,which was interrupted by both of PD123319 and AG490.Conclusions Transdifferentiarion of renal tubular epithelial cells occurs under acute ischemic- reperfusion injury.Local renin-angiotensin system may play a role in the transdifferentiation of TEC through AT2 receptor and its JAK2 signal pathway. 相似文献
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目的:了解广州市学龄前儿童乙肝疫苗的免疫效果,为乙肝疫苗加强免疫提供科学依据。方法:采用化学发光微粒子免疫分析法(CMIA)定量检测2 542名广州市0~6岁HBsAg阴性儿童血清抗-HBs浓度。结果:CMIA检测广州市0~6岁儿童血清抗-HBs总体阳性率为94.34%,随着年龄增长,血清抗-HBs阳性率逐渐降低,组间差异存在统计学意义(P<0.01);血清抗-HBs浓度亦逐渐下降,组间差异有统计学意义(P<0.01)。结论:广州市学龄前儿童乙肝免疫整体处于较高水平,但由于抗体的时效性,应定期检测血清抗-HBs浓度,及时复种加强免疫。 相似文献