Spinal cord injury (SCI) can lead to varying degrees of sensory and motor dysfunction. Salvianolic acid B (Sal-B) is the dominating bioactive constituent of Danshen, which has been reported to alleviate liver fibrosis and exert neuroprotective effects. But, the influence of Sal-B in SCI remains mysterious. The research planned to delve the protective function of Sal-B in hydrogen peroxide (H2O2)-caused PC-12 cell injury. H2O2-caused PC-12 cells injury model was built, CCK-8, Transwell and flow cytometry experiments were enforced to assess cell proliferation, migration and apoptosis. The microRNA (miR)-26a plasmid and the matching control were transfected into PC-12 cells, subsequently, the influence of miR-26a inhibition in H2O2-corrupted PC-12 cells was evaluated. The cell growth-correlated factors and PI3K/AKT and MEK/ERK pathways were assayed through western blot assay. Results corroborated that Sal-B eased H2O2-evoked injury in PC-12 cells. Ascended miR-26a was monitored in Sal-B and H2O2-exposed cells. MiR-26a inhibition annulled the protective action of Sal-B in H2O2-corrupted cells. The protective function of Sal-B was enabled through activating PI3K/AKT and MEK/ERK pathways. These findings delineated that Sal-B protected PC-12 cells against H2O2-caused injury through ascending miR-26a via initiating PI3K/AKT and MEK/ERK pathways. Highlights H2O2 causes PC-12 cell injury; Sal-B eases H2O2-caused PC-12 cell injury; Sal-B protects PC-12 cells against H2O2-caused injury via elevating miR-26a; Sal-B activates AKT and MEK/ERK pathways via modulating miR-26a.

中文翻译：

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丹酚酸B在PC-12细胞中通过介导microRNA-26a对过氧化氢引发的损伤的保护功能。

脊髓损伤（SCI）可能导致不同程度的感觉和运动功能障碍。丹酚酸B（Sal-B）是丹参的主要生物活性成分，据报道可减轻肝纤维化并发挥神经保护作用。但是，Sal-B在SCI中的影响仍然是神秘的。该研究计划研究Sal-B在过氧化氢（H2O2）引起的PC-12细胞损伤中的保护功能。建立了由H2O2引起的PC-12细胞损伤模型，并进行了CCK-8，Transwell和流式细胞术实验，以评估细胞的增殖，迁移和凋亡。将microRNA（miR）-26a质粒和匹配的对照转染到PC-12细胞中，随后评估miR-26a抑制对H2O2破坏的PC-12细胞的影响。通过western blot检测细胞生长相关因子以及PI3K / AKT和MEK / ERK途径。结果证实了Sal-B减轻了PC-12细胞中H2O2引起的损伤。在暴露于Sal-B和H2O2的细胞中监测上升的miR-26a。抑制MiR-26a消除了Sal-B在H2O2损坏的细胞中的保护作用。Sal-B的保护功能是通过激活PI3K / AKT和MEK / ERK途径实现的。这些发现表明，Sal-B通过启动PI3K / AKT和MEK / ERK途径使miR-26a升高，从而保护PC-12细胞免受H2O2引起的伤害。要点H2O2引起PC-12细胞损伤；Sal-B可减轻H2O2引起的PC-12细胞损伤；Sal-B通过升高miR-26a保护PC-12细胞免受H2O2引起的伤害。Sal-B通过调节miR-26a激活AKT和MEK / ERK途径。结果证实了Sal-B减轻了PC-12细胞中H2O2引起的损伤。在暴露于Sal-B和H2O2的细胞中监测上升的miR-26a。抑制MiR-26a消除了Sal-B在H2O2损坏的细胞中的保护作用。Sal-B的保护功能是通过激活PI3K / AKT和MEK / ERK途径实现的。这些发现表明，Sal-B通过启动PI3K / AKT和MEK / ERK途径使miR-26a升高，从而保护PC-12细胞免受H2O2引起的伤害。要点H2O2引起PC-12细胞损伤；Sal-B可减轻H2O2引起的PC-12细胞损伤；Sal-B通过升高miR-26a保护PC-12细胞免受H2O2引起的伤害。Sal-B通过调节miR-26a激活AKT和MEK / ERK途径。结果证实了Sal-B减轻了PC-12细胞中H2O2引起的损伤。在暴露于Sal-B和H2O2的细胞中监测上升的miR-26a。抑制MiR-26a消除了Sal-B在H2O2损坏的细胞中的保护作用。Sal-B的保护功能是通过激活PI3K / AKT和MEK / ERK途径实现的。这些发现表明，Sal-B通过启动PI3K / AKT和MEK / ERK途径使miR-26a升高，从而保护PC-12细胞免受H2O2引起的伤害。要点H2O2引起PC-12细胞损伤；Sal-B可减轻H2O2引起的PC-12细胞损伤；Sal-B通过升高miR-26a保护PC-12细胞免受H2O2引起的伤害。Sal-B通过调节miR-26a激活AKT和MEK / ERK途径。抑制MiR-26a消除了Sal-B在H2O2损坏的细胞中的保护作用。Sal-B的保护功能是通过激活PI3K / AKT和MEK / ERK途径实现的。这些发现表明，Sal-B通过启动PI3K / AKT和MEK / ERK途径使miR-26a升高，从而保护PC-12细胞免受H2O2引起的伤害。要点H2O2引起PC-12细胞损伤；Sal-B可减轻H2O2引起的PC-12细胞损伤；Sal-B通过升高miR-26a保护PC-12细胞免受H2O2引起的伤害。Sal-B通过调节miR-26a激活AKT和MEK / ERK途径。抑制MiR-26a消除了Sal-B在H2O2损坏的细胞中的保护作用。Sal-B的保护功能是通过激活PI3K / AKT和MEK / ERK途径实现的。这些发现表明，Sal-B通过启动PI3K / AKT和MEK / ERK途径使miR-26a升高，从而保护PC-12细胞免受H2O2引起的伤害。要点H2O2引起PC-12细胞损伤；Sal-B可减轻H2O2引起的PC-12细胞损伤；Sal-B通过升高miR-26a保护PC-12细胞免受H2O2引起的伤害。Sal-B通过调节miR-26a激活AKT和MEK / ERK途径。要点H2O2引起PC-12细胞损伤；Sal-B可减轻H2O2引起的PC-12细胞损伤；Sal-B通过升高miR-26a保护PC-12细胞免受H2O2引起的伤害。Sal-B通过调节miR-26a激活AKT和MEK / ERK途径。要点H2O2引起PC-12细胞损伤；Sal-B可减轻H2O2引起的PC-12细胞损伤；Sal-B通过升高miR-26a保护PC-12细胞免受H2O2引起的伤害。Sal-B通过调节miR-26a激活AKT和MEK / ERK途径。