Paeoniflorin Attenuates Inflammatory Pain by Inhibiting Microglial Activation and Akt-NF-κB Signaling in the Central Nervous System

被引:43
|
作者
Hu, Bo [1 ]
Xu, Guangtao [1 ]
Zhang, Xiaomin [2 ]
Xu, Long [1 ]
Zhou, Hong [1 ]
Ma, Zhenyi [1 ]
Shen, Xiaohua [1 ]
Zhu, Jia [1 ]
Shen, Ruilin [1 ]
机构
[1] Jiaxing Univ, Jiaxing Hosp Tradit Chinese Med, Inst Diabet & Nerve Dis, Dept Pathol, 501 East Zhongshan Rd, Jiaxing 31400, ZJ, Peoples R China
[2] Kunming Med Univ, Dept Physiol, Kunming, Yunnan, Peoples R China
基金
中国国家自然科学基金;
关键词
Paeoniflorin; Freund's complete adjuvant; Pain; Microglia; Akt; NF-kappa B; PROTEIN-INDUCING COMPOUND; NEUROPATHIC PAIN; SPINAL-CORD; RAT MODEL; INJURY; RECEPTORS; PHAGOCYTOSIS; CONSTITUENTS; CELLS; MICE;
D O I
10.1159/000490076
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Background/Aims: Paeoniflorin (PF) is known to have anti-inflammatory and paregoric effects, but the mechanism underlying its analgesic effect remains unclear. The aim of this study was to clarify the effect of PF on Freund's complete adjuvant (CFA)-induced inflammatory pain and explore the underlying molecular mechanism. Methods: An inflammatory pain model was established by intraplantar injection of CFA in C57BL/6J mice. After intrathecal injection of PF daily for 8 consecutive days, thermal and mechanical withdrawal thresholds, the levels of inflammatory factors TNF-alpha, IL-1 beta and IL-6, microglial activity, and the expression of Akt NF-kappa B signaling pathway in the spinal cord tissue were detected by animal ethological test, cell culture, enzyme-linked immunosorbent assay, immunofluorescence histochemistry, and western blot. Results: PF inhibited the spinal microglial activation in the CFA-induced pain model. The production of proinflammatory cytokines was decreased in the central nervous system after PF treatment both in vivo and in vitro. PF further displayed a remarkable effect on inhibiting the activation of Akt-NF-kappa B signaling pathway in vivo and in vitro. Conclusion: These results suggest that PF is a potential therapeutic agent for inflammatory pain and merits further investigation. (C) 2018 The Author(s) Published by S. Karger AG, Basel
引用
收藏
页码:842 / 850
页数:9
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