ABSTRACT

Objective

As an intravenous anesthetic, propofol has been exhibited to provide excellent clinical analgesia. Whether propofol has amelioration property for NP and neuroinflammation remains unexplored. The present study was arranged to probe the role of propofol in the mitigation of NP and neuroinflammation in rats and underlying mechanisms.

Methods

Rats were randomly classified into the following groups: Model, Sham, Control, Propofol, GW9662, and Saline groups. The radiant heat stimulation was used to measure paw withdrawal latency (PWL), and mechanical stimulation was employed to detect paw withdrawal threshold (PWT). Subsequently, the expression of GFAP was assessed by immunofluorescence to reflect the activation of astrocyte. qRT-PCR and Western blot were utilized for the performance of mRNA and protein expression levels of PPAR γ as well as inflammation factors (TNF-α, IL-1β, and IL-6).

Results

Pentobarbital sodium anesthesia significantly shortened the PWL and PWT, suppressed PPAR γ expression in rats in addition to elevating astrocyte activation and inflammation response. Propofol treatment attenuated the NP of rats as evidenced by restrained astrocyte activation level and inflammation factor levels. Rats treated with propofol had markedly heightened PPAR γ expression. PPAR γ exposure ameliorated NP and inflammation degree, which demonstrated by elevated astrocyte activation and inflammation levels as well as suppressed PWL and PWT in rats injected with PPAR γ inhibitor. Besides, PPAR γ decreased the expression level of β-catenin.

Conclusion

Propofol ameliorates NP and neuroinflammation of rats by up-regulating PPAR γ expression to block the Wnt/β-catenin pathway.

中文翻译：

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丙泊酚通过 PPAR γ 上调阻断 Wnt/β-catenin 通路来改善神经性疼痛和神经炎症。

摘要

客观的

作为一种静脉麻醉剂，丙泊酚已被证明可提供出色的临床镇痛。丙泊酚是否具有改善 NP 和神经炎症的特性尚待探索。本研究旨在探讨丙泊酚在减轻大鼠 NP 和神经炎症中的作用及其潜在机制。

方法

将大鼠随机分为以下组：模型组、假手术组、对照组、丙泊酚组、GW9662 组和盐水组。辐射热刺激用于测量缩爪潜伏期（PWL），并采用机械刺激来检测缩爪阈值（PWT）。随后，通过免疫荧光评估GFAP的表达以反映星形胶质细胞的活化。qRT-PCR 和蛋白质印迹用于检测 PPAR γ 的 mRNA 和蛋白质表达水平以及炎症因子（TNF-α、IL-1β 和 IL-6）。

结果

戊巴比妥钠麻醉显着缩短了 PWL 和 PWT，抑制了大鼠 PPAR γ 的表达，同时提高了星形胶质细胞的活化和炎症反应。丙泊酚治疗减弱了大鼠的 NP，这可以通过抑制星形胶质细胞活化水平和炎症因子水平来证明。用丙泊酚治疗的大鼠的 PPAR γ 表达显着增加。PPAR γ 暴露改善了 NP 和炎症程度，这通过星形胶质细胞活化和炎症水平升高以及注射 PPAR γ 抑制剂的大鼠的 PWL 和 PWT 得到抑制来证明。此外，PPAR γ 降低了 β-catenin 的表达水平。

结论

丙泊酚通过上调 PPAR γ 表达阻断 Wnt/β-catenin 通路来改善大鼠的 NP 和神经炎症。