Paeoniflorin attenuates the neuroinflammatory response in a rat model of chronic constriction injury

被引:39
作者
Zhou, Jianyu [1 ,2 ]
Wang, Jingxia [1 ]
Li, Wei [1 ]
Wang, Chenglong [1 ]
Wu, Li [1 ]
Zhang, Jianjun [1 ]
机构
[1] Beijing Univ Chinese Med, Sch Preclin Med, Dept Tradit Chinese Clin Pharmacol, 11 Beisanhuadonglu, Beijing 100029, Peoples R China
[2] Chengde Med Univ, Dept Tradit Chinese Med, Chengde 067000, Hebei, Peoples R China
基金
中国国家自然科学基金;
关键词
paeoniflorin; neuropathic pain; microglia; neuroinflammatory; proinflammatory cytokine; NF-KAPPA-B; PRIMARY AFFERENT NEURONS; NEUROPATHIC PAIN; SPINAL-CORD; SCIATIC-NERVE; SOFT CORAL; ACTIVATION; ALLODYNIA; MICROGLIA; INFLAMMATION;
D O I
10.3892/mmr.2017.6371
中图分类号
R73 [肿瘤学];
学科分类号
100214 [肿瘤学];
摘要
Neuropathic pain remains the most frequent cause of suffering and disability worldwide. Paeoniflorin (PF), a water-soluble monoterpene glycoside extracted from the roots of Paeonia lactiflora Pall, has a wide range of pharmacological functions. Although the neuroprotective effect of PF has been reported in animal models of neuropathology, no systematic investigation has reported on the analgesic properties of PF in neuropathic pain. The aim of the present study was to investigate whether PF can alleviate neuropathic pain and to examine its possible mechanism. Neuropathic pain was induced by chronic constriction injury (CCI) of the sciatic nerve in rats. Following CCI surgery, the rats were administered with PF for 11 days. Mechanical withdrawal threshold and thermal withdrawal latency were assessed prior to surgery, and on days 3, 7 and 11 post-surgery. The levels of interleukin (IL)-1 beta and tumor necrosis factor (TNF)-alpha in the spinal cord were analyzed using enzyme-linked immunosorbent assays. The activation of astrocytes and microglia were observed using immunostaining. In addition, the phosphorylation of p38 mitogen-alpha ctivated protein kinase (p-p38MAPK) and nuclear factor-kappa B (NF-kappa B) were examined using western blot analysis. The results indicated that PF significantly attenuated CCI-induced neuropathic pain and decreased the levels of TNF-alpha and IL-1 beta proinflammatory cytokines in the spinal cord. Furthermore, PF inhibited the over-activation of microglia and reduced the elevated expression levels of p-p38 MAPK and NF-kappa B in the spinal cord. These results indicated that PF offers potential as a therapeutic agent for neuropathic pain, which merits further investigation.
引用
收藏
页码:3179 / 3185
页数:7
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