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The Chinese Medicine Wu-Tou Decoction Relieves Neuropathic Pain by Inhibiting Hippocampal Microglia Activation.

ABSTRACT: The comorbidity between the nociceptive and mental syndromes adds to the refractoriness of neuropathic pain (NP). Wu-Tou decoction (WTD) has been prescribed for chronic pain for thousands of years in China. Recently, we reported that WTD was helpful for hippocampus and co-curative for the nociceptive, depressive and anxiety behaviors in the spinal cord ligation (SNL) mice. However, the mechanism underlying the rescue of hippocampus, as well as the roles hippocampus assumed in co-curation remain unexplored. In this study, we validated that in SNL mice, the long-lasting damages to limbic system were mainly limited to hippocampus. In addition, hippocampal neurons were proven sensitive to harms induced by microglia and rescued by WTD, which in sum indicated hippocampal microglia as the critical modulator of co-curation. To validate this hypothesis the hippocampal microglia were mal-activated in shamed mice, in which the atrophy of hippocampus and the development of NP syndromes were consolidated and proven rescued by WTD. On the contrary, in the SNL mice, the failure to control hippocampal microglia was sufficient to void all the rescues mediated by WTD. In sum, our study points out that the effective modulation of microglia in hippocampus is of pivotal importance for the co-curation by WTD.

SUBMITTER: Zhu C

PROVIDER: S-EPMC6095857 | biostudies-other | 2018 Aug

REPOSITORIES: biostudies-other

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The Chinese Medicine Wu-Tou Decoction Relieves Neuropathic Pain by Inhibiting Hippocampal Microglia Activation.

Zhu Chunyan C Xu Qionghong Q Mao Zhiyun Z Lin Na N

Scientific reports 20180816 1

The comorbidity between the nociceptive and mental syndromes adds to the refractoriness of neuropathic pain (NP). Wu-Tou decoction (WTD) has been prescribed for chronic pain for thousands of years in China. Recently, we reported that WTD was helpful for hippocampus and co-curative for the nociceptive, depressive and anxiety behaviors in the spinal cord ligation (SNL) mice. However, the mechanism underlying the rescue of hippocampus, as well as the roles hippocampus assumed in co-curation remain ...[more]

PMID: 30115941

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Project description:BackgroundNeuropathic pain is caused by sensory nerve injury, but effective treatments are currently lacking. Microglia are activated in the spinal dorsal horn after sensory nerve injury and contribute to neuropathic pain. Accordingly, molecules expressed by these cells are considered potential targets for therapeutic strategies. Our previous gene screening study using a mouse model of motor nerve injury showed that the G-protein-coupled receptor 34 gene (GPR34) is induced by nerve injury. Because GPR34 is now considered a microglia-enriched gene, we explored the possibility that it might be involved in microglial activation in the dorsal horn in a mouse model of neuropathic pain.MethodsmRNA expression of GPR34 and pro-inflammatory molecules was determined by quantitative real-time PCR in wild-type and GPR34-deficient mice with L4 spinal nerve injury. In situ hybridization was used to identify GPR34 expression in microglia, and immunohistochemistry with the microglial marker Iba1 was performed to examine microglial numbers and morphology. Mechanical sensitivity was evaluated by the von Frey hair test. Liquid chromatography-tandem mass spectrometry quantified expression of the ligand for GPR34, lysophosphatidylserine (LysoPS), in the dorsal horn, and a GPR34 antagonist was intrathecally administrated to examine the effect of inhibiting LysoPS-GPR34 signaling on mechanical sensitivity.ResultsGPR34 was predominantly expressed by microglia in the dorsal horn after L4 nerve injury. There were no histological differences in microglial numbers or morphology between WT and GPR34-deficient mice. However, nerve injury-induced pro-inflammatory cytokine expression levels in microglia and pain behaviors were significantly attenuated in GPR34-deficient mice. Furthermore, the intrathecal administration of the GPR34 antagonist reduced neuropathic pain.ConclusionsInhibition of GPR34-mediated signal by GPR34 gene deletion reduced nerve injury-induced neuropathic pain by suppressing pro-inflammatory responses of microglia without affecting their morphology. Therefore, the suppression of GPR34 activity may have therapeutic potential for alleviating neuropathic pain.

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The Chinese Medicine Wu-Tou Decoction Relieves Neuropathic Pain by Inhibiting Hippocampal Microglia Activation.

Publications

The Chinese Medicine Wu-Tou Decoction Relieves Neuropathic Pain by Inhibiting Hippocampal Microglia Activation.

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