Evidence map›Paper›PMID 42404422›Full record

ArticleBasic and clinical neuroscience2025

Impact of Genotropin on Oxidative Stress, Glutamate, and Nitric Oxide Pathways in a Rat Model of Peripheral Neuropathy.

Sepideh Saffarpour, Arash Mehraz, Pargol Sadeghi Tehran, Farinaz Nasirinezhad

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In one paragraph

Article in Basic and clinical neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Sepideh SaffarpourDepartment of Orthopedics, Bone and Joint Reconstruction Research Center, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-5824-5399
Arash MehrazPhysiology Research Center, Iran University of Medical Sciences, Tehran, Iran.
Pargol Sadeghi TehranCellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.
Farinaz NasirinezhadCellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-4404-4780

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Genotropin, a recombinant human growth hormone (GH), has been proposed as a potential repositioning drug to treat neurological disorders. However, its efficacy in managing neuropathic pain remains unclear. This study aimed to evaluate the analgesic effects of Genotropin and investigate its potential mechanisms of action. Methods: Two weeks after chronic constriction injury (CCI) of the sciatic nerve, adult male rats were randomly assigned to three main groups: Control, vehicle (normal saline [NS]), and treatment. The treatment group received Genotropin at doses of 0.3 and 0.6 mg/kg, either alone or in combination with L-arginine, L-NAME, or glutamate (n=8 per group). Pain-related behaviors were assessed using Von Frey filaments, the plantar test, and the Randall-Selitto test. Blood samples were collected to analyze oxidative and antioxidative markers. Results: Genotropin significantly reduced mechanical allodynia (P<0.05, F=2.7) and mechanical (P<0.01, F=3.4) and thermal hyperalgesia (P<0.001, F=2.5). Pretreatment with 0.3 mg/kg GH abolished the pronociceptive effects of L-arginine (500 mg/kg) and glutamate (1000 nmol) (P<0.01; F=2, F=3) while enhancing the antinociceptive effect of L-NAME (P<0.05, F=2.8). GH also significantly reduced lipid peroxidation (P<0.01, F=3.7) and restored levels of glutathione, glutathione peroxidase (GPx), and superoxide dismutase (SOD) (P<0.01; F=11, F=10.52, F=5, respectively). Additionally, catalase (CAT) levels were significantly increased (P<0.01, F=5). Conclusion: These results suggest that exogenous GH alleviates neuropathic pain and enhances antioxidant defenses in a model of peripheral neuropathic pain. The involvement of glutamate and nitric oxide (NO) pathways in GH's antinociceptive effects was also demonstrated. Therefore, Genotropin holds potential as a repositioned therapeutic agent for treating neuropathic pain.

Indexed as

GlutamateGrowth hormone (Genotropin)Neuropathic painNitric oxide (NO)Oxidative factors

Identifiers

PMID42404422
PMCPMC13332375

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