ArticleInternational journal of clinical and experimental pathology2014
Omega-conotoxin MVIIC attenuates neuronal apoptosis in vitro and improves significant recovery after spinal cord injury in vivo in rats.
Article in International journal of clinical and experimental pathology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 17 citations in OpenAlex.
- Protective Effect of Peptide Calcium Channel Blocker Omega-Hexatoxin-Hv1a on Epithelial Cell during Ischemia-Reperfusion Injury.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Potential Active Marine Peptides as Anti-Aging Drugs or Drug Candidates.Marine drugs · 2023Review
- Effect of the Peptide Calcium Channel Blocker ω-hexatoxin-Hv1a on Cell Death during Ischemia/ReperfusionSovremennye tekhnologii v meditsine · 2023Article
- Pathophysiological Responses to Conotoxin Modulation of Voltage-Gated Ion Currents.Marine drugs · 2022Review
- Management of thoracic spinal cord injury in a professional American football athlete: illustrative case.Journal of neurosurgery. Case lessons · 2021Article
- Protein Degradome of Spinal Cord Injury: Biomarkers and Potential Therapeutic Targets.Molecular neurobiology · 2020Review
- Conotoxin MVIIA improves cell viability and antioxidant system after spinal cord injury in rats.PloS one · 2018Article
- Animal Toxins as Therapeutic Tools to Treat Neurodegenerative Diseases.Frontiers in pharmacology · 2018Review
- Withaferin A protects against spinal cord injury by inhibiting apoptosis and inflammation in mice.Pharmaceutical biology · 2017Article
- Ligustilide treatment promotes functional recovery in a rat model of spinal cord injury via preventing ROS production.International journal of clinical and experimental pathology · 2015Article
- Modification of HSP proteins and Ca2+ are responsible for the NO-derived peroxynitrite mediated neurological damage in PC12 cell.International journal of clinical and experimental pathology · 2015Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive accumulation of intracellular calcium is the most critical step after spinal cord injury (SCI). Reducing the calcium influx should result in a better recovery from SCI. Calcium channel blockers have been shown a great potential in reducing brain and spinal cord injury. In this study, we first tested the neuroprotective effect of MVIIC on slices of spinal cord subjected to ischemia evaluating cell death and caspase-3 activation. Thereafter, we evaluated the efficacy of MVIIC in ameliorating damage following SCI in rats, for the first time in vivo. The spinal cord slices subjected a pretreatment with MVIIC showed a cell protection with a reduction of dead cells in 24.34% and of caspase-3-specific protease activation. In the in vivo experiment, Wistar rats were subjected to extradural compression of the spinal cord at the T12 vertebral level using a weigh of 70 g/cm, following intralesional treatment with either placebo or MVIIC in different doses (15, 30 and 60 pmol) five minutes after injury. Behavioral testing of hindlimb function was done using the Basso Beattie Bresnahan locomotor rating scale, and revealed significant recovery with 15 pmol (G15) compared to other trauma groups. Also, histological bladder structural revealed significant outcome in G15, with no morphological alterations, and anti-NeuN and TUNEL staining showed that G15 provided neuron preservation and indicated that this group had fewer neuron cell death, similar to sham. These results showed the neuroprotective effects of MVIIC in in vitro and in vivo model of SCI with neuronal integrity, bladder and behavioral improvements.
Indexed as
Identifiers
25120731PMC4128966W1905964504What 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.