摘要
目的探讨急性肺血栓栓塞(PTE)患者血浆刺激血管内皮细胞对eNOS及HSP90表达的影响,进一步了解NO产生的机制。方法分别用正常人血浆和PTE患者血浆刺激人脐静脉血管内皮细胞(HUVEC),哥尔德霉素(Geldanamycin)抑制HSP90的作用后,以硝酸还原酶法测定各组细胞培养上清NO浓度,免疫组织化学法测定脐静脉内皮细胞eNOS及HSP90表达水平。结果加入PTE患者血浆处理HUVEC组eNOS及HSP90表达水平较加入正常人血浆处理组增强;PTE患者血浆处理HUVEC组NO浓度为(16.62±3.14)μmol/L,正常人血浆处理组NO浓度为(5.16±1.98)μmol/L,经统计学分析两组差异有统计学意义(t=13.2,P<0.05)。哥尔德霉素处理组NO浓度为(9.34±1.09)μmol/L,明显低于PTE患者血浆处理组,差异有统计学意义(t=15.6,P<0.05)。结论PTE患者血浆可以刺激血管内皮细胞eNOS及HSP90表达上调;HSP90的抑制剂哥尔德霉素可以通过抑制HSP90从而下调NO的产生。
Objective To explore the effect of PTE patients blood plasm on the protein expression of eNOS and HSP90 in endothelial cells and the mechanism of produce nitric oxide （ NO）. Methods Human umbilical vein endothelial cells were cultured with PIE patients blood plasm（ experiment group） and normal people blood plasm （control group）, the NO concentration in cultured cell supernatant were detenninned with nitrate reductase method, The expression of HSP90 and eNOS protein were detected by immunocytochemistry, the NO production was also measured after using Geldanamycin to block the action of HSP90. Results The expression of HSP90 and eNOS protein in experiment group were higher than that in control group; the NO concentration [ （ 16.62 ± 3.14）μmol/L] in experiment group was significantly higher than that in control group [（5.16 ± 1.98 ）μmol/L], （t = 13.2, P 〈 0. 05） , the NO concentration in the Geldanamycin treated group was 9.34 ± 1.09μmol/L, compared with the experiment group, the distinction was obvious（ t = 15.6, P 〈 0. 05）. Conclusion PIE patients blood plasm can up- regulate the expression of eNOS and HSP90 protein in endothelial cell, Blocking the role of HSP90 can reduce production of NO.
出处
《中国急救医学》
CAS
CSCD
北大核心
2006年第6期401-403,共3页
Chinese Journal of Critical Care Medicine
基金
国家自然科学基金资助项目(No.50347009)
