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首页> 外文期刊>Acta Pharmacologica Sinica >Interleukin-1 beta induction of neuron apoptosis depends on p38 mitogen-activated protein kinase activity after spinal cord injury
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Interleukin-1 beta induction of neuron apoptosis depends on p38 mitogen-activated protein kinase activity after spinal cord injury

机译：脊髓损伤后白介素-1β诱导神经元凋亡取决于p38丝裂原激活的蛋白激酶活性

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Aim: Interleukin-1 beta (IL-1β) has been implicated as an extracellular signal in the initiation of apoptosis in neurons and oligodendrocytes after spinal cord injury (SCI). To further characterize the apoptotic cascade initiated by IL-1β after SCI, we examined the expression of IL-1β, p38 mitogen-activated protein kinase (p38 MAPK) and caspase-3 after SCI, and further investigated whether p38 MAPK was involved in neuron apoptosis induced by IL-1β. Methods: Adult rats were given contusion SCI at the T-10 vertebrae level with a weight-drop impactor (10 g weight dropped 25.0 mm). The expression levels of IL-1β, p38 MAPK and caspase-3 after SCI were assessed with Western blots, immunohistochemistry staining, and real time reverse transcription polymerase chain reactions (RT-PCR). Neuron apoptosis was assessed with the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick end labeling (TUNEL) method. Results: Increased levels of IL-1β and p38 MAPK were observed soon after injury, with a peak in expression levels within 6 h of injury. By 24 h after injury, caspase-3 expression was markedly increased in the injured spinal cord. TUNEL-positive cells were first observed in the lesioned area 6 h after SCI. The largest number of TUNEL-positive cells was observed at 24 h post-SCI. Intrathecal injection of the IL-1 receptor antagonist IL-1Ra significantly reduced expression of p38 MAPK and caspase-3, and reduced the number of TUNEL-positive cells. Moreover, intrathecal injection of an inhibitor of p38 MAPK, SB203580, also significantly reduced the expression of caspase-3, and reduced the number of TUNEL-positive cells in the injured spinal cord. Conclusion: The p38MAPK signaling pathway plays an important role in IL-1β mediated induction of neuron apoptosis following SCI in rats.
机译：目的：白介素-1（IL-1β）已被认为是脊髓损伤（SCI）后神经元和少突胶质细胞凋亡启动中的一种细胞外信号。为了进一步表征SCI后由IL-1β引发的凋亡级联反应，我们检查了SCI后IL-1β，p38丝裂原活化蛋白激酶（p38 MAPK）和caspase-3的表达，并进一步研究了p38 MAPK是否参与神经元。 IL-1β诱导的细胞凋亡。方法：给成年大鼠在T-10椎骨上用减重撞击器（10克重25.0毫米）挫伤SCI。通过蛋白质印迹，免疫组织化学染色和实时逆转录聚合酶链反应（RT-PCR）评估SCI后IL-1β，p38 MAPK和caspase-3的表达水平。用末端脱氧核苷酸转移酶介导的三磷酸脱氧尿苷-生物素缺口末端标记（TUNEL）方法评估神经元凋亡。结果：损伤后不久发现IL-1β和p38 MAPK水平升高，在损伤后6小时内表达水平达到峰值。到损伤后24小时，在受伤的脊髓中caspase-3表达明显增加。脊髓损伤后6小时，在病变区域首先观察到TUNEL阳性细胞。在SCI后24小时观察到最大数量的TUNEL阳性细胞。鞘内注射IL-1受体拮抗剂IL-1Ra可显着降低p38 MAPK和caspase-3的表达，并减少TUNEL阳性细胞的数量。此外，鞘内注射p38 MAPK抑制剂SB203580也显着降低了caspase-3的表达，并减少了受损脊髓中TUNEL阳性细胞的数量。结论：p38MAPK信号通路在大鼠脊髓损伤后IL-1β介导的神经元凋亡诱导中起重要作用。

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