Changes of Cervical Dorsal Root Ganglia Induced by Compression Injury and Decompression Procedure: A Novel Rat Model of Cervical Radiculoneuropathy

Zhan-ying, Tang; Shu, Bing; Cui, Xue‐jun; Zhou, Chong-Jian; Shi, Qi; Holz, Jonathan D.; Wang, Yongjun

doi:10.1089/neu.2008.0506

Cited by 15 publications

(10 citation statements)

References 22 publications

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“…It is thus possible that mechanical stresses activate neuronal TRPV1 channels via the PLA 2 -12-HPETE pathway to induce the mechanical hypersensitivity of afferent nerves. Consistent with this idea, recent studies reported that the expression level of PLA 2 in DRG neurons was significantly elevated following compression injury or inflammation [51], [52]. Whether this pathway would contribute to the development of DMA in vivo will be an intriguing topic of the future study.…”

Section: Discussionmentioning

confidence: 57%

Spatio-Temporal Expression and Functional Involvement of Transient Receptor Potential Vanilloid 1 in Diabetic Mechanical Allodynia in Rats

Cui

et al. 2014

PLoS ONE

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Diabetic neuropathic pain (DNP) is one of the most common clinical manifestations of diabetes mellitus (DM), which is characterized by prominent mechanical allodynia (DMA). However, the molecular mechanism underlying it has not fully been elucidated. In this study, we examined the spatio-temporal expression of a major nociceptive channel protein transient receptor potential vanilloid 1 (TRPV1) and analyzed its functional involvement by intrathecal (i.t.) application of TRPV1 antagonists in streptozocin (STZ)-induced DMA rat models. Western blot and immunofluorescent staining results showed that TRPV1 protein level was significantly increased in the soma of the dorsal root ganglion (DRG) neurons on 14 days after STZ treatment (DMA 14 d), whereas those in spinal cord and skin (mainly from the central and peripheral processes of DRG neurons) had already been enhanced on DMA 7 d to peak on DMA 14 d. qRT-PCR experiments confirmed that TRPV1 mRNA level was significantly up-regulated in the DRG on DMA 7 d, indicating a preceding translation of TRPV1 protein in the soma but preferential distribution of this protein to the processes under the DMA conditions. Cell counting assay based on double immunostaining suggested that increased TRPV1-immunoreactive neurons were likely to be small-sized and CGRP-ergic. Finally, single or multiple intrathecal applications of non-specific or specific TRPV1 antagonists, ruthenium red and capsazepine, at varying doses, effectively alleviated DMA, although the effect of the former was more prominent and long-lasting. These results collectively indicate that TRPV1 expression dynamically changes during the development of DMA and this protein may play important roles in mechanical nociception in DRG neurons, presumably through facilitating the release of CGRP.

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Section: Discussionmentioning

confidence: 57%

Spatio-Temporal Expression and Functional Involvement of Transient Receptor Potential Vanilloid 1 in Diabetic Mechanical Allodynia in Rats

Cui

et al. 2014

PLoS ONE

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“…Clinical studies revealed that QSP can significantly improve mild-to-moderate NP and improve the quality of life of patients with mild-tomoderate NP, especially concerning physiological function, social function, emotional function, vitality, and other aspects. In a number of randomized, double-blind, placebocontrolled studies, improvements in dysfunction associated with mild-to-moderate NP were observed in both the QSP and placebo group, although the improvement was significantly better in the QSP group [5]. To study the mechanism of action of QSP, this study relied on the TCMSP and BATMAN-TCM platforms to study the active constituents e results of this study suggest that QSP most likely exerts its therapeutic effects on NP through interactions among MOL021, MOL001, PTGS2, and PTGS1, thereby laying a foundation for subsequent confirmatory studies.…”

Section: Discussionmentioning

confidence: 98%

“…Qi She Pill (QSP) has been approved by the China Food and Drug Administration (approval number: Z20090978), and it is widely available in China [5]. QSP is composed of six Chinese herbs, namely Caulis Sinomenii (CS, Qing Feng Teng), Calculus Bovis (BC, Niu Huang), Chuanxiong Rhizoma (CR, Chuan Xiong), Stephaniae Tetrandrae Radix (STR, Fang Ji), Hedysarum Multijugum Maxim (HMM, Huang Qi), and Moschus (MO, She Xiang).…”

Section: Introductionmentioning

confidence: 99%

An Analysis of the Anti‐Neuropathic Effects of Qi She Pill Based on Network Pharmacology

Song

Bao

Zhou

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Background. Qi She Pill (QSP) is a traditional prescription for the treatment of neuropathic pain (NP) that is widely used in China. However, no network pharmacology studies of QSP in the treatment of NP have been conducted to date. Objective. To verify the potential pharmacological effects of QSP on NP, its components were analyzed via target docking and network analysis, and network pharmacology methods were used to study the interactions of its components. Materials and Methods. Information on pharmaceutically active compounds in QSP and gene information related to NP were obtained from public databases, and a compound-target network and protein-protein interaction network were constructed to study the mechanism of action of QSP in the treatment of NP. The mechanism of action of QSP in the treatment of NP was analyzed via Gene Ontology (GO) biological process annotation and Kyoto Gene and Genomics Encyclopedia (KEGG) pathway enrichment, and the drug-like component-target-pathway network was constructed. Results. The compound-target network contained 60 compounds and 444 corresponding targets. The key active compounds included quercetin and beta-sitosterol. Key targets included PTGS2 and PTGS1. The protein-protein interaction network of the active ingredients of QSP in the treatment of NP featured 48 proteins, including DRD2, CHRM, β2-adrenergic receptor, HTR2A, and calcitonin gene-related peptide. In total, 53 GO entries, including 35 biological process items, 7 molecular function items, and 11 cell related items, were identified. In addition, eight relevant (KEGG) pathways were identified, including calcium, neuroactive ligand-receptor interaction, and cAMP signaling pathways. Conclusion. Network pharmacology can help clarify the role and mechanism of QSP in the treatment of NP and provide a foundation for further research.

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“…It has been reported that the restoration of lumbar intervertebral foramen space improves mechanical hypersensitivity and that decompression of the DRG reduces compression-induced decreases of DRG neurons [ 41 ]. Thus, it is possible to expect that gradual attenuation of CCD-induced mechanical hypersensitivity is due to the recovery of damaged CCD neurons by the gradual widening of the intervertebral foramen over a period of time after injury.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Spinal GABAergic Inhibition and Mechanical Hypersensitivity following Chronic Compression of Dorsal Root Ganglion in the Rat

et al. 2015

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Chronic compression of dorsal root ganglion (CCD) results in neuropathic pain. We investigated the role of spinal GABA in CCD-induced pain using rats with unilateral CCD. A stereological analysis revealed that the proportion of GABA-immunoreactive neurons to total neurons at L4/5 laminae I–III on the injured side decreased in the early phase of CCD (post-CCD week 1) and then returned to the sham-control level in the late phase (post-CCD week 18). In the early phase, the rats showed an increase in both mechanical sensitivity of the hind paw and spinal WDR neuronal excitability on the injured side, and such increase was suppressed by spinally applied muscimol (GABA-A agonist, 5 nmol) and baclofen (GABA-B agonist, 25 nmol), indicating the reduced spinal GABAergic inhibition involved. In the late phase, the CCD-induced increase in mechanical sensitivity and neuronal excitability returned to pre-CCD levels, and such recovered responses were enhanced by spinally applied bicuculline (GABA-A antagonist, 15 nmol) and CGP52432 (GABA-B antagonist, 15 nmol), indicating the regained spinal GABAergic inhibition involved. In conclusion, the alteration of spinal GABAergic inhibition following CCD and leading to a gradual reduction over time of CCD-induced mechanical hypersensitivity is most likely due to changes in GABA content in spinal GABA neurons.

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Changes of Cervical Dorsal Root Ganglia Induced by Compression Injury and Decompression Procedure: A Novel Rat Model of Cervical Radiculoneuropathy

Cited by 15 publications

References 22 publications

Spatio-Temporal Expression and Functional Involvement of Transient Receptor Potential Vanilloid 1 in Diabetic Mechanical Allodynia in Rats

Spatio-Temporal Expression and Functional Involvement of Transient Receptor Potential Vanilloid 1 in Diabetic Mechanical Allodynia in Rats

An Analysis of the Anti‐Neuropathic Effects of Qi She Pill Based on Network Pharmacology

Modulation of Spinal GABAergic Inhibition and Mechanical Hypersensitivity following Chronic Compression of Dorsal Root Ganglion in the Rat

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