 英语晨读 · 山东省立医院疼痛科英语晨读已经坚持10余年的时间了，每天交班前15分钟都会精选一篇英文文献进行阅读和翻译。一是可以保持工作后的英语阅读习惯，二是可以学习前沿的疼痛相关知识。我们会将晨读内容与大家分享，助力疼痛学习。 本次文献选自Francesca Guidaa，Monica Iannottaa，Gabriella Misso, et al. Pain. 2022.本次学习由李芸主治医师主讲。 3.8. Spared nerve injury corresponds with distinct proinflammatory altered gene expression patterns in the prefrontal cortex and hippocampus We next investigated whether SNI was associated with changes in gene expression in the brain regions known to be involved in affective components of chronic pain. The expression levels of 96 genes, including cytokines, chemokines, growth factors, and several markers, were analysed in both hippocampus and PFC of the 1-month and 12-month SNI mice and related controls (Figs. 5 and 6). In detail, tissue samples were pooled for each category based on the brain area, age, and condition and then processed for mRNA microfluidic TaqMan array using Mouse Immune Panel. The relative gene expression in the 1-month and 12-month sham mice revealed 34 more than 2.5-fold upmodulated genes in hippocampus and 15 ones in PFC (Fig. 5A and B). Data elaboration by PANTHER classification system revealed, for the hippocampal pattern, 8 genes sharing a common involvement in inflammation mediated by either chemokine or cytokine signaling pathway (Fig. S3A, available at http://links./PAIN/B547). Among these, in addition to proinflammatory chemokines and cytokines Chemokine (C-C motif) ligand 19 (CCL19); C-X-C motif chemokine ligand 10 (CXCL10); Interleukin-15 (IL-15); Interleukin-18 (IL-18) (CCL19, CXCL10, IL15, and IL18), stands out the 5.1 and 14.9 upregulation of nuclear factor NF-kappa-B (NFKB1) and inhibitor of nuclear factor kappa B kinase subunit beta (IKBKB), respectively. Pathway enrichment analysis also revealed the involvement of 5 genes in apoptosis signaling pathway, 4 genes in cholecystokinin receptor (CCKR) signaling pathway, and 3 genes in JAK/STAT pathway. Among the most regulated genes, we also observed b2-microglobulin (B2M, 10.6-fold), the complement component C3 (23.8-fold), CC chemokine receptor 2 (CCR2, 8.3-fold), CD38 (15.4-fold), H2-Eb1 (16.3-fold), hypoxanthine phosphoribosyltransferase 1 (HPRT1) (26.6-fold), leucocyte marker PTPRC (CD45, 13.6-fold), and suppressor of cytokine signaling 2 (SOCS2) (39.5-fold). 3.8. SNI影响海马和PFC促炎因子相关基因的表达 我们接下来研究了SNI是否与已知参与慢性疼痛情感成分的大脑区域的基因表达变化有关。我们分析了1个月和12个月的SNI小鼠和相关对照组的海马和PFC中96个基因的表达水平，包括细胞因子、趋化因子、生长因子和一些标志物（图5和6）。详细地说，根据脑区、年龄和条件，对每一类组织样本进行汇总，然后进行mRNA微流控TaqMan阵列处理。1个月和12个月的假手术组的基因表达显示，海马区有34个超过2.5倍的上调基因，PFC有15个（图5A和B）。通过PANTHER分类系统的数据阐述，发现在海马区中，有8个基因共同参与了由趋化因子或细胞因子信号通路介导的炎症（图S3）。其中，除了促炎趋化因子和细胞因子外，还有CCL19、CXCL10、IL-15、IL-18、NFKB1、IKBKB的上调。富集分析还显示有5个基因参与了细胞凋亡信号通路，4个基因参与了胆囊收缩素受体（CCKR）信号通路，3个基因参与了JAK/STAT通路。受调控最多的基因包括b2-微球蛋白（B2M，10.6倍），补体成分C3（23.8倍），CC趋化因子受体2（CCR2，8.3倍），CD38（15. 4倍），H2-Eb1（16.3倍），次黄嘌呤磷酸核苷转移酶1（HPRT1）（26.6倍），白细胞标志物PTPRC（CD45，13.6倍）和细胞因子信号转导抑制因子2（SOCS2）（39.5倍）。
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