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目的研究高原驻训部队返回人员炎症因子失衡的变化及其意义。方法对21名长期居住平原地区(海拔200 m),平均25岁,初上高原前身体健康,驻训6个月返回后出现高原脱适应症的男性官兵,在上高原前(Control)、返回平原第2天(d2)及第30天(d30)分别抽取空腹静脉血,分离血清,-80℃冻存,ELISA法检测上述返回人员血清中IL-17A及IL-10的含量。结果 d2及d30时间点IL-17A含量及IL-17A/IL-10比率较Control有显著增高(P<0.05),d30时间点IL-17A含量及IL-17A/IL-10比率低于d2时间点(P<0.05);d2及d30时间点IL-10的含量较Control有显著降低(P<0.05),但d30时间点IL-10含量高于d2时间点(P<0.05)。在Control、d2、d30时间点IL-10与IL-17A存在呈正相关(r1=0.948,P<0.05;r2=0.969,P<0.05;r3=0.972,P<0.05);IL-10与IL-17A在d2与Control间、d30与d2间的改变量呈负相关(r4=-0.793,P<0.05;r5=-0.756,P<0.05)。结论高原驻训部队返回人员机体中存在炎症因子失衡的现象,其程度随着返回平原时间的延长而减弱,其炎症因子失衡有所恢复,但其具体机制仍需进一步研究。
Objective To study the changes and their significance of the imbalance of inflammatory cytokines among returning personnel in the troops stationed in the plateau. Methods Twenty-one male officers and men with altitude alopecia after 21 months of long-term living plains (average elevation of 200 m), average 25 years old, healthy before beginning of the plateau, returned to their homeland after 6 months’ training returned to the plateau (Control) Fasting venous blood was drawn on day 2 (d2) and day 30 (d30) respectively. Serum was separated and frozen at -80 ℃. The contents of IL-17A and IL-10 in sera of the returned persons were detected by ELISA. Results The levels of IL-17A and the ratio of IL-17A / IL-10 at d2 and d30 were significantly higher than those at Control (P <0.05), and the levels of IL-17A and IL-17A / IL-10 at d30 were lower than those at d2 (P <0.05). The content of IL-10 at d2 and d30 was significantly lower than that at Control (P <0.05), but the level of IL-10 at d30 was higher than that at d2 (P <0.05). There was a positive correlation between IL-10 and IL-17A at the time of Control, d2 and d30 (r1 = 0.948, P <0.05; r2 = 0.969, 17A showed a negative correlation between d30 and d2 (r4 = -0.793, P <0.05; r5 = -0.756, P <0.05) between d2 and Control. Conclusions There is an imbalance of inflammatory cytokines in the returning personnel of the troops stationed in the plateau. The degree of inflammation is weakened with the prolongation of return to the plain, and the imbalance of inflammatory cytokines recovered. However, the specific mechanism needs further study.