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目的:肌萎缩侧索硬化(amyotrophic lateral sclerosis,ALS)疾病进展过程中,趋化因子(fractalkine,FKN)对受损的运动神经元可能起保护作用,但有关ALS患者血浆FKN表达的研究还未见报道,本文对FKN在ALS患者病程中的免疫炎症机制做初步研究,探索该指标是否可以成为潜在的血浆生物学标志,尝试寻找治疗ALS的新方法。方法:采用MILLIPLEX MAP液相芯片技术,检测51例ALS患者与60例正常对照的血浆FKN水平,按性别、病程、起病部位、疾病严重程度分组,研究患者与正常对照组血浆FKN水平。结果:患者的血浆FKN水平比正常对照低(P<0.05),分析表明:各亚组患者血浆FKN水平均比正常对照低(P均<0.05);病程>12个月患者的FKN水平比病程≤12个月的患者高(P<0.05),其余亚组之间FKN水平差异均无统计学意义(P均>0.05);另外,患者的血浆FKN水平与病程无统计相关性(P>0.05)。结论:患者的血浆FKN水平比正常对照低,提示其与ALS可能有一定关联,具体作用机制还有待今后深入探索。
OBJECTIVE: Fractalkine (FKN) may play a protective role in injured motor neurons during the development of amyotrophic lateral sclerosis (ALS). However, the study on the expression of FKN in plasma of ALS patients has not been studied yet See reports, this article on FKN ALS patients in the pathogenesis of immune inflammation preliminary study to explore whether the index can become a potential biomarker of plasma, try to find a new method of treatment of ALS. Methods: Plasma FKN levels in 51 patients with ALS and 60 normal controls were detected by MILLIPLEX MAP liquid-phase microarray. Plasma FKN levels in patients and controls were studied by gender, course of disease, onset site and severity of disease. Results: Plasma FKN levels in patients were lower than those in normal controls (P <0.05). Analysis showed that FKN levels in all subgroups were lower than those in normal controls (all P <0.05). FKN levels in patients with duration of> 12 months were significantly lower than those in normal controls (P <0.05). There was no significant difference in the level of FKN among the other subgroups (P> 0.05). In addition, there was no significant correlation between the level of FKN and the course of disease (P> 0.05) ). Conclusions: The plasma FKN level in patients is lower than that in normal controls, suggesting that there may be a correlation between the level of FKN and ALS. The specific mechanism remains to be explored in the future.