ArticleInternational journal of clinical and experimental medicine2015
Fasudil alleviates traumatic optic neuropathy by inhibiting Rho signaling pathway.
Article in International journal of clinical and experimental medicine, 2015. 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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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Adjunctive use of netarsudil 0.02% in the treatment of refractory glaucoma: a one year analysis.International ophthalmology · 2024Article
- Immunological and molecular basics of the primary open angle glaucoma pathomechanism.Central-European journal of immunology · 2021Review
- Fasudil attenuates glial cell-mediated neuroinflammation via ERK1/2 and AKT signaling pathways after optic nerve crush.Molecular biology reports · 2020Article
- Role of the Rho GTPase/Rho kinase signaling pathway in pathogenesis and treatment of glaucoma: Bench to bedside research.Experimental eye research · 2017Review
- Fasudil inhibits LPS-induced migration of retinal microglial cells via regulating p38-MAPK signaling pathway.Molecular vision · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesThe present study is to investigate the pathological changes in rabbits with traumatic optic neuropathy (TON), as well as the effect of fasudil on the lesions.
methodsA total of 144 New Zealand rabbits were successfully established as TON models. Twelve hours after surgery, the rabbits in control, dexamethasone, and fasudil groups were administrated with saline, dexamethasone, and fasudil via ear veins, respectively. Then, retinas of the rabbits were obtained at 72 h and on days 7, 14 and 21 after surgery. The pathological changes in retina and optic nerves were observed by hematoxylin and eosin staining and transmission electron microscopy. The expression levels of Rho-associated genes were measured using quantitative real-time polymerase chain reaction.
resultsIn control group, the axons were swelling, and mitochondria showed vacuolation after optic nerve crush. Mitochondria were swelled slightly in dexamethasone group. By contrast, nerves in fasudil group were repaired. Retinal ganglion cells in control group were reduced significantly due to optic nerve crush. The loss of retinal ganglion cells was alleviated in fasudil group. Quantitative real-time polymerase chain reaction showed that the expression of Rho-associated genes were down-regulated.
conclusionsThe present study demonstrates that fasudil inhibits the apoptosis of retinal ganglion cells and ameliorates damages of optic nerves in traumatic optic neuropathy.
Indexed as
Identifiers
26550269PMC4612954W2411305886What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.