ArticleMolecular medicine reports2017
Effect of fasudil on cognitive function following status convulsion in rats.
Article in Molecular medicine reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 11 citations in OpenAlex.
- Intermittent theta-burst stimulation alleviates hypoxia-ischemia-caused myelin damage and neurologic disability.Experimental neurology · 2024Article
- Effect of the ROCK inhibitor fasudil on the brain proteomic profile in the tau transgenic mouse model of Alzheimer's disease.Frontiers in aging neuroscience · 2024Article
- Role of Rho-associated kinases and their inhibitor fasudil in neurodegenerative diseases.Frontiers in neuroscience · 2024Review
- The Effect of Short-Term Feeding of a High-Coconut Oil or High-Fat Diet on Neuroinflammation and the Performance of an Object-Place Task in Rats.Neurochemical research · 2021Article
- The Role and Mechanism of AMIGO3 in the Formation of Aberrant Neural Circuits After Status Convulsion in Immature Mice.Frontiers in molecular neuroscience · 2021Article
- Antidepressant-relevant behavioral and synaptic molecular effects of long-term fasudil treatment in chronically stressed male rats.Neurobiology of stress · 2020Article
- Dexmedetomidine Attenuates Neurotoxicity in Developing Rats Induced by Sevoflurane through Upregulating BDNF-TrkB-CREB and Downregulating ProBDNF-P75NRT-RhoA Signaling Pathway.Mediators of inflammation · 2020Article
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6 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Fasudil has been demonstrated to possess a protective effect in neural injury; however, its protective effect on convulsive brain injury remains to be assessed. The aim of the present study was to investigate the latent mechanism and effect of fasudil on cognitive function following status convulsion (SC) in rats. Initially, to determine the effects of SC, the expression levels of Ras homolog gene family, member A (RhoA)/Rho‑associated protein kinase (ROCK) signaling pathway‑associated proteins were measured by western blot analysis in 16 rats. To investigate the effects of fasudil on cognitive function in SC rats, a further 40 rats were assigned to four groups: Group I (healthy untreated rats), group II (healthy rats treated with fasudil), group III (SC rats) and group IV (SC rats treated with fasudil). An object‑in‑place memory task and the Morris Water Maze test were subsequently performed. Histopathological alterations in brain tissue and SC latency were additionally analyzed. Following SC, protein expression levels of myelin‑associated glycoprotein, myelin oligodendrocyte glycoprotein and leucine rich repeat and immunoglobulin‑like domain‑containing protein 1 were significantly increased (P<0.05) and levels of neurite outgrowth inhibitor protein A were significantly decreased (P<0.01). SC had no effect on RhoA level (P=0.921); however, it significantly increased the levels of phosphorylated RhoA (P<0.01). Cognitive function was significantly decreased following SC and significantly increased following fasudil intervention. Fasudil intervention improved CA1 structure, which was lost following SC. SC severely impaired cognitive function and affected the expression of neurite growth inhibitory factors. Fasudil treatment improved cognitive function and central nervous system (CNS) injury, and decreased SC susceptibility in rats. Fasudil and SC may regulate the CNS by affecting the expression of neurite growth inhibitory factors in the RhoA/ROCK signaling pathway.
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