论文部分内容阅读
目的：观察反义肿瘤坏死因子－α（ｔｕｍｏｒｎｅｃｒｏｓｉｓｆａｃｔｏｒ－ａｌｐｈａ，ＴＮＦ－α）寡脱氧核苷酸对ＬＰＳ诱导的感染性休克小鼠的影响，为采用反义技术降低感染性休克死亡率的早期临床试验奠定基础。方法：通过腹腔注射ＬＰＳ建立感染性休克小鼠模型。采用腹腔注射方法，通过ＤＯＴＡＰ转染导入系统，使反义ＴＮＦ－α寡脱氧核苷酸（ｏｌｉｇｏｄｅｏｘｙｎｕｃｌｅｏｔｉｄｅ，ＯＤＮ）作用于小鼠单核吞噬细胞系统；采用ＲＴ－ＰＣＲ，ＥＬＩＳＡ检测ＴＮＦ－α的ｍＲＮＡ和蛋白质的表达水平。结果：反义ＴＮＦ－αＯＤＮ降低了ＬＰＳ诱导的感染性休克小鼠的ＴＮＦ－α的释放，降低了感染性休克小鼠的死亡率，而正义ＴＮＦ－αＯＤＮ和错配ＴＮＦ－αＯＤＮ与对照组相比，对ＴＮＦ－α的释放无影响，未能降低感染性休克小鼠的死亡率。结论：反义ＴＮＦ－αＯＤＮ以序列特异性方式抑制了ＬＰＳ诱导的感染性休克小鼠的ＴＮＦ－α的释放，降低了感染性休克小鼠的死亡率。
OBJECTIVE: To observe the effect of antisense tumor necrosis factor-α (TNF-α) oligodeoxynucleotides on LPS-induced septic shock in mice, and to use antisense technology to reduce septic shock mortality in early stage Test laid the foundation. Methods: Septic shock mice were established by intraperitoneal injection of LPS. The antisense TNF-α oligodeoxynucleotide (ODN) was applied to the mouse mononuclear phagocyte system by intraperitoneal injection and DOTAP transfection. The mRNA of TNF-α was detected by RT-PCR and ELISA And protein expression level. RESULTS: Antisense TNF-αODN reduced the release of TNF-α in septic shock mice induced by LPS and decreased the mortality of septic shock mice. The levels of TNF-αODN and mismatch TNF-αODN in control group Compared with the release of TNF-α had no effect, failed to reduce the mortality of septic shock mice. CONCLUSION: Antisense TNF-αODN inhibits the release of TNF-α in LPS-induced septic shock mice in a sequence-specific manner and reduces the mortality of septic shock mice.