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  1. Article ; Online: αO-Conotoxin GeXIVA[1,2] Reduced Neuropathic Pain and Changed Gene Expression in Chronic Oxaliplatin-Induced Neuropathy Mice Model.

    Wang, Huanbai / Li, Xiaodan / Qiao, Yamin / Wang, Meiting / Wang, Wen / McIntosh, J Michael / Zhangsun, Dongting / Luo, Sulan

    Marine drugs

    2024  Volume 22, Issue 1

    Abstract: Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting painful neuropathy that occurs commonly during cancer management, which often leads to the discontinuation of medication. Previous studies suggest that the α9α10 nicotinic acetylcholine ...

    Abstract Chemotherapy-induced peripheral neuropathy (CIPN) is a dose-limiting painful neuropathy that occurs commonly during cancer management, which often leads to the discontinuation of medication. Previous studies suggest that the α9α10 nicotinic acetylcholine receptor (nAChR)-specific antagonist αO-conotoxin GeXIVA[1,2] is effective in CIPN models; however, the related mechanisms remain unclear. Here, we analyzed the preventive effect of GeXIVA[1,2] on neuropathic pain in the long-term oxaliplatin injection-induced CIPN model. At the end of treatment, lumbar (L4-L6) spinal cord was extracted, and RNA sequencing and bioinformatic analysis were performed to investigate the potential genes and pathways related to CIPN and GeXIVA[1,2]. GeXIVA[1,2] inhibited the development of mechanical allodynia induced by chronic oxaliplatin treatment. Repeated injections of GeXIVA[1,2] for 3 weeks had no effect on the mice's normal pain threshold or locomotor activity and anxiety-like behavior, as evaluated in the open field test (OFT) and elevated plus maze (EPM). Our RNA sequencing results identified 209 differentially expressed genes (DEGs) in the CIPN model, and simultaneously injecting GeXIVA[1,2] with oxaliplatin altered 53 of the identified DEGs. These reverted genes were significantly enriched in immune-related pathways represented by the cytokine-cytokine receptor interaction pathway. Our findings suggest that GeXIVA[1,2] could be a potential therapeutic compound for chronic oxaliplatin-induced CIPN management.
    MeSH term(s) Mice ; Animals ; Oxaliplatin/adverse effects ; Conotoxins/pharmacology ; Neuralgia/chemically induced ; Neuralgia/drug therapy ; Neuralgia/genetics ; Hyperalgesia/chemically induced ; Hyperalgesia/drug therapy ; Hyperalgesia/genetics ; Disease Models, Animal ; Nicotinic Antagonists/pharmacology ; Gene Expression ; Antineoplastic Agents/adverse effects
    Chemical Substances Oxaliplatin (04ZR38536J) ; Conotoxins ; Nicotinic Antagonists ; Antineoplastic Agents
    Language English
    Publishing date 2024-01-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2175190-0
    ISSN 1660-3397 ; 1660-3397
    ISSN (online) 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md22010049
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Novel αO-conotoxin GeXIVA[1,2] Nonaddictive Analgesic with Pharmacokinetic Modelling-Based Mechanistic Assessment.

    Zhu, Xiaoyu / Yuan, Mei / Wang, Huanbai / Zhangsun, Dongting / Yu, Gang / Che, Jinjing / Luo, Sulan

    Pharmaceutics

    2022  Volume 14, Issue 9

    Abstract: αO-conotoxin GeXIVA[1,2] was isolated in our laboratory ... ...

    Abstract αO-conotoxin GeXIVA[1,2] was isolated in our laboratory from
    Language English
    Publishing date 2022-08-26
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527217-2
    ISSN 1999-4923
    ISSN 1999-4923
    DOI 10.3390/pharmaceutics14091789
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: The α9α10 Nicotinic Acetylcholine Receptor Antagonist αO-Conotoxin GeXIVA[1,2] Alleviates and Reverses Chemotherapy-Induced Neuropathic Pain

    Wang, Huanbai / Li, Xiaodan / Zhangsun, Dongting / Yu, Gang / Su, Ruibin / Luo, Sulan

    Marine drugs. 2019 May 05, v. 17, no. 5

    2019  

    Abstract: Oxaliplatin is a third-generation platinum drug and is widely used as a first-line therapy for the treatment of colorectal cancer (CRC). However, a large number of patients receiving oxaliplatin develop dose-limiting painful neuropathy. Here, we report ... ...

    Abstract Oxaliplatin is a third-generation platinum drug and is widely used as a first-line therapy for the treatment of colorectal cancer (CRC). However, a large number of patients receiving oxaliplatin develop dose-limiting painful neuropathy. Here, we report that αO-conotoxin GeXIVA[1,2], a highly potent and selective antagonist of the α9α10 nicotinic acetylcholine receptor (nAChR) subtype, can relieve and reverse oxaliplatin-induced mechanical and cold allodynia after single and repeated intramuscular (IM) injections in rats. Treatments were started at 4 days post oxaliplatin injection when neuropathic pain emerged and continued for 8 and 16 days. Cold score and mechanical paw withdrawal threshold (PWT) were detected by the acetone test and von Frey test respectively. GeXIVA[1,2] significantly relieved mechanical and cold allodynia in oxaliplatin-treated rats after a single injection. After repeated treatments, GeXIVA[1,2] produced a cumulative analgesic effect without tolerance and promoted recovery from neuropathic pain. Moreover, the long lasting analgesic effect of GeXIVA[1,2] on mechanical allodynia continued until day 10 after the termination of the 16-day repeated treatment procedure. On the contrary, GeXIVA[1,2] did not affect acute mechanical and thermal pain behaviors in normal rats after repeated injections detected by the von Frey test and tail flick test. GeXIVA[1,2] had no influence on rat hind limb grip strength and body weight after repeated treatments. These results indicate that αO-conotoxin GeXIVA[1,2] could provide a novel strategy to treat chemotherapy-induced neuropathic pain.
    Keywords acetone ; analgesic effect ; antagonists ; body weight ; cold ; colorectal neoplasms ; drugs ; hindlimbs ; nicotinic receptors ; pain ; patients ; peripheral nervous system diseases ; physical activity ; platinum ; rats ; tail flick test ; therapeutics
    Language English
    Dates of publication 2019-0505
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ZDB-ID 2175190-0
    ISSN 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md17050265
    Database NAL-Catalogue (AGRICOLA)

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  4. Article ; Online: The α9α10 Nicotinic Acetylcholine Receptor Antagonist αO-Conotoxin GeXIVA[1,2] Alleviates and Reverses Chemotherapy-Induced Neuropathic Pain.

    Wang, Huanbai / Li, Xiaodan / Zhangsun, Dongting / Yu, Gang / Su, Ruibin / Luo, Sulan

    Marine drugs

    2019  Volume 17, Issue 5

    Abstract: Oxaliplatin is a third-generation platinum drug and is widely used as a first-line therapy for the treatment of colorectal cancer (CRC). However, a large number of patients receiving oxaliplatin develop dose-limiting painful neuropathy. Here, we report ... ...

    Abstract Oxaliplatin is a third-generation platinum drug and is widely used as a first-line therapy for the treatment of colorectal cancer (CRC). However, a large number of patients receiving oxaliplatin develop dose-limiting painful neuropathy. Here, we report that αO-conotoxin GeXIVA[1,2], a highly potent and selective antagonist of the α9α10 nicotinic acetylcholine receptor (nAChR) subtype, can relieve and reverse oxaliplatin-induced mechanical and cold allodynia after single and repeated intramuscular (IM) injections in rats. Treatments were started at 4 days post oxaliplatin injection when neuropathic pain emerged and continued for 8 and 16 days. Cold score and mechanical paw withdrawal threshold (PWT) were detected by the acetone test and von Frey test respectively. GeXIVA[1,2] significantly relieved mechanical and cold allodynia in oxaliplatin-treated rats after a single injection. After repeated treatments, GeXIVA[1,2] produced a cumulative analgesic effect without tolerance and promoted recovery from neuropathic pain. Moreover, the long lasting analgesic effect of GeXIVA[1,2] on mechanical allodynia continued until day 10 after the termination of the 16-day repeated treatment procedure. On the contrary, GeXIVA[1,2] did not affect acute mechanical and thermal pain behaviors in normal rats after repeated injections detected by the von Frey test and tail flick test. GeXIVA[1,2] had no influence on rat hind limb grip strength and body weight after repeated treatments. These results indicate that αO-conotoxin GeXIVA[1,2] could provide a novel strategy to treat chemotherapy-induced neuropathic pain.
    MeSH term(s) Analgesics/pharmacology ; Animals ; Conotoxins/pharmacology ; Disease Models, Animal ; Hyperalgesia/drug therapy ; Male ; Neuralgia/chemically induced ; Neuralgia/drug therapy ; Oxaliplatin/administration & dosage ; Oxaliplatin/adverse effects ; Oxaliplatin/antagonists & inhibitors ; Rats ; Rats, Sprague-Dawley
    Chemical Substances Analgesics ; Conotoxins ; alpha-conotoxin, Conus generalis ; Oxaliplatin (04ZR38536J)
    Language English
    Publishing date 2019-05-05
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2175190-0
    ISSN 1660-3397 ; 1660-3397
    ISSN (online) 1660-3397
    ISSN 1660-3397
    DOI 10.3390/md17050265
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Wnt1/β-catenin signaling upregulates spinal VGLUT2 expression to control neuropathic pain in mice.

    Zhang, Zhi-Ling / Yu, Gang / Peng, Jing / Wang, Huan-Bai / Li, Yu-Lei / Liang, Xiao-Nan / Su, Rui-Bin / Gong, Ze-Hui

    Neuropharmacology

    2019  Volume 164, Page(s) 107869

    Abstract: Vesicular glutamate transporter 2 (VGLUT2)-which uptakes glutamate into presynaptic vesicles-is a fundamental component of the glutamate neurotransmitter system. Although several lines of evidence from genetically modified mice suggest a possible ... ...

    Abstract Vesicular glutamate transporter 2 (VGLUT2)-which uptakes glutamate into presynaptic vesicles-is a fundamental component of the glutamate neurotransmitter system. Although several lines of evidence from genetically modified mice suggest a possible association of VGLUT2 with neuropathic pain, the specific role of VGLUT2 in the spinal cord during neuropathic pain, and its regulatory mechanism remain elusive. In this study, we report that spared nerve injury induced an upregulation of VGLUT2 in the spinal cord, and intrathecal administration of small hairpin RNAs (shRNA) against VGLUT2 before or after surgery attenuated mechanical allodynia, and pathologically-enhanced glutamate release. Meanwhile, nerve injury activated the Wnt1/β-catenin signaling pathway in a quick-onset and sustained manner, and blocking the Wnt1 signaling with a Wnt1 targeting antibody attenuated neuropathic pain. In naïve mice, administration of a Wnt agonist or Wnt1 increased spinal VGLUT2 protein levels. Moreover, intrathecal administration of the Wnt/β-catenin inhibitor, XAV939 attenuated mechanical allodynia, and this effect was concurrent with that of VGLUT2 downregulation. Pretreatment with VGLUT2 shRNAs abolished the allodynia induced by the Wnt agonist or Wnt1. These findings reveal a novel mechanism wherein there is Wnt1/β-catenin-dependent VGLUT2 upregulation in neuropathic pain, thus potentiating the development of new therapeutic strategies in pain management.
    MeSH term(s) Animals ; Glutamic Acid/metabolism ; Hyperalgesia/drug therapy ; Immunohistochemistry ; Injections, Spinal ; Male ; Mice ; Mice, Inbred C57BL ; Neuralgia/physiopathology ; RNA, Small Interfering/administration & dosage ; RNA, Small Interfering/therapeutic use ; Spinal Cord/drug effects ; Spinal Cord/metabolism ; Synaptosomes/drug effects ; Synaptosomes/metabolism ; Up-Regulation ; Vesicular Glutamate Transport Protein 2/biosynthesis ; Wnt Signaling Pathway/drug effects ; beta Catenin/metabolism
    Chemical Substances CTNNB1 protein, mouse ; RNA, Small Interfering ; Slc17a6 protein, mouse ; Vesicular Glutamate Transport Protein 2 ; beta Catenin ; Glutamic Acid (3KX376GY7L)
    Language English
    Publishing date 2019-11-27
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218272-5
    ISSN 1873-7064 ; 0028-3908
    ISSN (online) 1873-7064
    ISSN 0028-3908
    DOI 10.1016/j.neuropharm.2019.107869
    Database MEDical Literature Analysis and Retrieval System OnLINE

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