Chronic constriction injury (CCI) of the sciatic nerve was used to establish neuropathic pain (NP) models in rats. CCI rats were then treated with propofol (Pro) and their paw withdrawal mechanical threshold (PWMT) and paw withdrawal thermal latency (PWTL) were measured. In addition, the expression patterns of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-10 were detected. CCI rats treated with propofol were further injected with antagomiR-140-3p to verify the role of miR-140-3p in propofol's analgesic actions. In addition to confirming the relationship between miR-140-3p and JAG1, the expression patterns of JAG1 itself were detected. Propofol-treated CCI rats were also injected with Ad-JAG1 (adenovirus-packaged JAG1 overexpression vector and Ad-NC) to test the role of JAG1 in propofol's analgesic mechanism of action. Finally, the levels of JAG1 and Notch pathway-related proteins were detected

中文翻译：

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丙泊酚通过 microRNA-140-3p/Jagged-1 肽/Notch 信号通路减轻慢性缩窄性损伤大鼠模型的神经性疼痛

使用坐骨神经慢性收缩损伤（CCI）建立大鼠神经性疼痛（NP）模型。然后用丙泊酚 (Pro) 治疗 CCI 大鼠并测量它们的缩爪机械阈值 (PWMT) 和缩爪热潜伏期 (PWTL)。此外，还检测了肿瘤坏死因子-α（TNF-α）、白细胞介素-1β（IL-1β）和IL-10的表达模式。用丙泊酚治疗的CCI大鼠进一步注射antagomiR-140-3p，以验证miR-140-3p在丙泊酚镇痛作用中的作用。除了确认 miR-140-3p 和 JAG1 之间的关系外，还检测了 JAG1 本身的表达模式。丙泊酚治疗的 CCI 大鼠也注射了 Ad-JAG1（腺病毒包装的 JAG1 过表达载体和 Ad-NC），以测试 JAG1 在丙泊酚镇痛作用机制中的作用。