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Neuroprotective effects of autophagy induced by rapamycin in rat acute spinal cord injury model

机译：雷帕霉素诱导的自噬对大鼠急性脊髓损伤的神经保护作用

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Background/Aims: To explore the effects of rapamycin-induced autophagy on apoptosis in a rat model of acute spinal cord injury (SCI), and to explore the effect of rapamycin on apoptosis in primary spinal cord cell culture. Methods: SCI was induced at T10 in female adult Sprague-Dawley rats. After injury was induced, the rats were injected with rapamycin and/or methylprednisolone and were sacrificed at various days after injury. Apoptosis and autophagy were examined with TUNEL staining and electron microscopy. Hind limb function was assessed by the Gale scale. Results: The expression of the apoptosis-related protein caspase-3 did not significantly increase until 21 days following injury, while increases in LC3II and LC3I began 10 days after injury, but then declined. TUNEL staining and electron microscopy confirmed that following injury autophagy occurred before apoptosis, but by 14 days after the injury, the level of autophagy had decreased significantly while the level of apoptosis showed a continued increase. Following treatment with rapamycin, apoptosis was significantly higher than in the vehicle control group, but significantly lower than in the sham-operated group, showing a protective effect of rapamycin. Gale scale grades in rats treated with rapamycin were significantly higher compared with the vehicle control group, suggesting a functional effect of rapamycin-induced inhibition of apoptosis. Conclusions: The results indicate that rapamycin significantly improved the prognosis of acute SCI in rats by inhibiting cell apoptosis. Rapamycin might be useful as a therapeutic agent for acute SCI.
机译：背景/目的：探讨雷帕霉素诱导的自噬对急性脊髓损伤（SCI）大鼠模型中细胞凋亡的影响，并探讨雷帕霉素对原代脊髓细胞培养中细胞凋亡的影响。方法：在成年Sprague-Dawley成年大鼠的T10诱导SCI。诱导损伤后，给大鼠注射雷帕霉素和/或甲基泼尼松龙，并在损伤后数天处死。通过TUNEL染色和电子显微镜检查细胞凋亡和自噬。后肢功能通过大风量表评估。结果：凋亡相关蛋白caspase-3的表达直到损伤后21天才显着增加，而LC3II和LC3I的表达在损伤后10天开始增加，但随后下降。 TUNEL染色和电镜观察证实，损伤后自噬发生在细胞凋亡之前，但是到损伤后14天，自噬水平显着下降，而细胞凋亡水平则持续上升。用雷帕霉素治疗后，细胞凋亡明显高于媒介物对照组，但明显低于假手术组，显示出雷帕霉素的保护作用。与载体对照组相比，雷帕霉素治疗的大鼠的大风等级等级明显更高，表明雷帕霉素诱导的细胞凋亡抑制作用具有功能性。结论：结果表明雷帕霉素可通过抑制细胞凋亡而显着改善大鼠急性SCI的预后。雷帕霉素可能用作急性SCI的治疗剂。

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