ArticleInvestigative ophthalmology & visual science2024
Growth Hormone Neuroprotective Effects After an Optic Nerve Crush in the Male Rat.
Article in Investigative ophthalmology & visual science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Dysregulation of neurovascular unit in the retina after optic nerve injury.BMC ophthalmology · 2026Article
- Tracer Techniques in Ophthalmology: Ocular Applications and Systemic Connections.Diagnostics (Basel, Switzerland) · 2026Review
- Role of Growth Hormone (GH) and Other Somatotropic Axis Elements in Retinal Neuroprotection.Current issues in molecular biology · 2026Review
- Positive Evolution of a Child Suffering from Caudal Regression Syndrome and Agenesia Sacra After Treatment with Growth Hormone and Rehabilitation.International journal of molecular sciences · 2025Article
- Growth hormone reduces retinal inflammation and preserves microglial morphology after optic nerve crush in male rats.Frontiers in cellular neuroscience · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Growth hormone (GH) has neuroprotective effects that have not been evaluated in the mammalian visual system. This study tested the hypothesis that GH administration can promote retinal neuroprotection in an optic nerve crush (ONC) model in male rats. Methods: The ON was compressed for 10 seconds, and bovine GH was injected concomitantly to injury for 14 days (0.5 µg/g every 12 hours). At 24 hours and 14 days after ONC, we evaluated the effects of GH upon several markers by quantitative PCR (qPCR), Western blot, and immunohistochemistry; the ON integrity was assessed using CTB Alexa 488 anterograde tracer, and retinal function was tested by full-field electroretinogram. Results: GH partially prevented the ONC-induced death of retinal ganglion cells (RGCs), as well as the increase in gliosis marker GFAP at 14 days. Most of the ONC-induced changes in mRNA retinal levels of several neurotrophic, survival, synaptogenic, gliosis, and excitotoxicity markers were prevented by GH, both at 24 hours and 14 days, and treatment also stimulated the expression of antiapoptotic proteins Bcl-2 and Bcl-xL at 24 hours. Additionally, GH partially maintained the ON integrity and active anterograde transport, as well as retinal function by avoiding the reduced amplitude and slowing of the A- and B-waves and oscillatory potentials associated with the ONC at 14 days. Conclusions: GH has neuroprotective effects in the ONC model in male rats, it promoted RGC survival, gliosis reduction, and axonal transport increase, likely through the regulation of genes involved in neuroprotection, survival, and synaptogenesis. Furthermore, GH prevented functional impairment, indicating its potential as a therapeutic option for retinal neurodegenerative diseases.
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Registered trials
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