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      Journal of Pain Research (submit here)

      This international, peer-reviewed Open Access journal by Dove Medical Press focuses on reporting of high-quality laboratory and clinical findings in all fields of pain research and the prevention and management of pain. Sign up for email alerts here.

      52,235 Monthly downloads/views I 2.832 Impact Factor I 4.5 CiteScore I 1.2 Source Normalized Impact per Paper (SNIP) I 0.655 Scimago Journal & Country Rank (SJR)

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      Systemic Injection of Thalidomide Prevent and Attenuate Neuropathic Pain and Alleviate Neuroinflammatory Response in the Spinal Dorsal Horn

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          Abstract

          Background and objective

          Thalidomide (Tha) has been shown to exert immunomodulatory and anti-inflammatory properties. Whether Tha can alleviate spinal nerve ligation (SNL)-induced neuropathic pain (NP) is still unclear. This study aimed to investigate the therapeutic effect of Tha on the SNL-induced NP and further explore the potential analgesic mechanisms of Tha.

          Methods

          The effects of Tha on SNL-induced mechanical allodynia were assessed by pain behavioral testing. The expressions of the astrocyte marker glial fibrillary acidic protein (GFAP) and the microglia marker Iba1 in the spinal dorsal horn were evaluated by immunofluorescence histochemistry. Protein expressions of the tumor necrosis factor alpha (TNF-α) in the spinal dorsal horn were tested by Western blot assay. Data were analyzed using one-way ANOVA or two-way ANOVA.

          Results

          By the pretreatment with a single intraperitoneal injection, the PWMT in SNL+Tha group was significantly increased from day 1 to day 2 after SNL ( P < 0.05 compared with SNL+Veh group). By the posttreatment with a single intraperitoneal injection, the PWMT in SNL+Tha group was also significantly increased from day 3 to day 4 after SNL ( P < 0.05 compared with SNL+Veh group). By the posttreatment with multiple intraperitoneal injection, both the PWMT and the PWTL in SNL+Tha group were similarly significantly increased from day 3 to day 14 after SNL ( P < 0.05 compared with SNL+Veh group). Furthermore, the GFAP and Iba1 expressions and TNF-α levels of the ipsilateral spinal dorsal horn in SNL+Tha group were significantly weaker from day 3 to day 14 after SNL than those in SNL+Veh group ( P < 0.05).

          Conclusion

          Tha can significantly alleviate NP induced by SNL. The analgesic mechanism may be related to inhibition of astrocyte and microglia activation as well as down-regulation of TNF-α levels in the spinal dorsal horn.

          Most cited references28

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          Mechanisms of Chemotherapy-Induced Peripheral Neuropathy

          Renata Zajączkowska, Magdalena Kocot-Kępska, Wojciech Leppert … (2019)
          Chemotherapy-induced peripheral neuropathy (CIPN) is one of the most frequent side effects caused by antineoplastic agents, with a prevalence from 19% to over 85%. Clinically, CIPN is a mostly sensory neuropathy that may be accompanied by motor and autonomic changes of varying intensity and duration. Due to its high prevalence among cancer patients, CIPN constitutes a major problem for both cancer patients and survivors as well as for their health care providers, especially because, at the moment, there is no single effective method of preventing CIPN; moreover, the possibilities of treating this syndrome are very limited. There are six main substance groups that cause damage to peripheral sensory, motor and autonomic neurons, which result in the development of CIPN: platinum-based antineoplastic agents, vinca alkaloids, epothilones (ixabepilone), taxanes, proteasome inhibitors (bortezomib) and immunomodulatory drugs (thalidomide). Among them, the most neurotoxic are platinum-based agents, taxanes, ixabepilone and thalidomide; other less neurotoxic but also commonly used drugs are bortezomib and vinca alkaloids. This paper reviews the clinical picture of CIPN and the neurotoxicity mechanisms of the most common antineoplastic agents. A better understanding of the risk factors and underlying mechanisms of CIPN is needed to develop effective preventive and therapeutic strategies.
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            Current challenges in glia-pain biology.

            Stephen McMahon, Marzia Malcangio (2009)
            A remarkable series of findings over the last decade or so has demonstrated a previously unrecognized role for CNS glia in many aspects of neuronal functioning including pain processing. In addition to their recruitment to sites of CNS damage, these cells also appear to be capable of "action at a distance," playing functional roles in areas of CNS that are quite remote from the focus of injury or disease. The implication is that the nervous system is able to initiate signals that alter the function of these glial cells, and these cells in turn release factors that regulate neuronal function. This idea has taken root, resulting in an explosion of research interest, and here we look critically at what has been reported in order to assess where knowledge is missing or uncertain.
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              Free radical-mediated oxidative DNA damage in the mechanism of thalidomide teratogenicity.

              P. S. Wells, T Parman, Leanne Wiley (1999)
              The sedative drug thalidomide ([+]-alpha-phthalimidoglutarimide), once abandoned for causing birth defects in humans, has found new therapeutic license in leprosy and other diseases, with renewed teratological consequences. Although the mechanism of teratogenesis and determinants of risk remain unclear, related teratogenic xenobiotics are bioactivated by embryonic prostaglandin H synthase (PHS) to a free-radical intermediates that produce reactive oxygen species (ROS), which cause oxidative damage to DNA and other cellular macromolecules. Similarly, thalidomide is bioactivated by horseradish peroxidase, and oxidizes DNA and glutathione, indicating free radical-mediated oxidative stress. Furthermore, thalidomide teratogenicity in rabbits is reduced by the PHS inhibitor acetylsalicylic acid, indicating PHS-catalyzed bioactivation. Here, we show in rabbits that thalidomide initiates embryonic DNA oxidation and teratogenicity, both of which are abolished by pre-treatment with the free radical spin trapping agent alpha-phenyl-N-t-butylnitrone (PBN). In contrast, in mice, a species resistant to thalidomide teratogenicity, thalidomide does not enhance DNA oxidation, even at a dose 300% higher than that used in rabbits, providing insight into an embryonic determinant of species-dependent susceptibility. In addition to their therapeutic implications, these results constitute direct evidence that the teratogenicity of thalidomide may involve free radical-mediated oxidative damage to embryonic cellular macromolecules.
              Article 0 comments Cited 62 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Pain Res
                Journal ID (iso-abbrev): J Pain Res
                Journal ID (publisher-id): JPR
                Journal ID (pmc): jpainres
                Title: Journal of Pain Research
                Publisher: Dove
                ISSN (Electronic): 1178-7090
                Publication date (Electronic): 29 November 2019
                Publication date Collection: 2019
                Volume: 12
                Pages: 3221-3230
                Affiliations
                [1 ]Department of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University , Xi’an, Shaan Xi, People’s Republic of China
                [2 ]Institution of Basic Medical Science, Xi’an Medical University , Xi’an, Shaan Xi, People’s Republic of China
                [3 ]Department of Anesthesiology, Shaanxi Provincial Cancer Hospital , Xi’an, Shaan Xi, People’s Republic of China
                [4 ]The Key Laboratory of Biomedical Information Engineering of the Ministry of Education, School of Life Science and Technology, Xi’an Jiaotong University , Xi’an, Shaan Xi, People’s Republic of China
                [5 ]Department of Anesthesiology, The First Affiliated Hospital of Xi’an Jiaotong University , Xi’an, Shaan Xi, People’s Republic of China
                Author notes
                Correspondence: Yun-Qing Li; Yu-Peng Feng Department of Anatomy, Histology and Embryology, K.K. Leung Brain Research Centre, The Fourth Military Medical University , Xi’an, Shaan Xi, People’s Republic of China Email deptanat@fmmu.edu.cn; fengyp@fmmu.edu.cn
                [*]

                These authors contributed equally to this work

                Author information
                http://orcid.org/0000-0002-4033-7180
                Article
                Publisher ID: 213112
                DOI: 10.2147/JPR.S213112
                PMC ID: 6896366
                SO-VID: 000a639b-7d9e-419c-86e9-ef2fcaba6fab
                Copyright © © 2019 Xu et al.
                License:

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                History
                Date received : 24 April 2019
                Date accepted : 07 November 2019
                Page count
                Figures: 7, References: 30, Pages: 10
                Categories
                Subject: Original Research

                ScienceOpen disciplines: Anesthesiology & Pain management
                Keywords: tha,neuropathic pain,glia,tnf-α,spinal nerve ligation
                Data availability:
                ScienceOpen disciplines: Anesthesiology & Pain management
                Keywords: tha, neuropathic pain, glia, tnf-α, spinal nerve ligation

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