Evidence map›Paper›PMID 35693152›Full record

ArticleBasic and clinical neuroscience

Hepatocyte Growth Factor Attenuates the Severity of Status Epilepticus in Kainic Acid-induced Model of Temporal Lobe Epilepsy by Targeting Apoptosis and Astrogliosis.

Sobhan Haghani, Nida Jamali-Raeufy, Motahareh Zeinivand, Soraya Mehrabi, Leila Aryan, Javad Fahanik-Babaei

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Article in Basic and clinical neuroscience. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 54% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 4 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Sobhan HaghaniDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0002-5993-0742
Nida Jamali-RaeufyDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-2416-0335
Motahareh ZeinivandDepartment of Physiology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran.ORCID https://orcid.org/0000-0002-0556-9525
Soraya MehrabiDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0001-8555-726X
Leila AryanDepartment of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0003-3795-0520
Javad Fahanik-BabaeiElectrophysiology Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.ORCID https://orcid.org/0000-0001-6707-132X
Iran University of Medical Sciences · IRKermanshah University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Although pharmacotherapy is the most common treatment for epilepsy, proper seizure control is not achieved with current medications. This study evaluated the protective effects of the Hepatocyte Growth Factor (HGF) in a rat model of Temporal Lobe Epilepsy (TLE) and explored possible molecular mechanisms. Methods: A TLE rat model was determined using an intra-hippocampal kainic acid injection (4 μg). Intra-cerebrovascular injection of HGF (6 μg) was performed 30 min before kainic acid injection. Learning and memory impairment were investigated by behavioral tests. The Enzyme-Linked Immunosorbent (ELISA) was used to determine astrogliosis and DNA fragmentation. Changes in neuronal density and mossy fiber sprouting were evaluated by Nissl and Timm staining, respectively. Results: Behavioral assessments indicated that kainate-treated rats presented spontaneous seizures. Moreover, their alternation percentage scores in the Y-Maze test were lower (P<0.001). Likewise, the passive avoidance test confirmed learning disability in Kainate-treated rats (P<0.001). HGF administration reduced the number of spontaneous seizures, alternation percentage score (P<0.001), and cognitive disturbances (P<0.001). The histopathological results also showed that a protected HGF administration contributed to the reduction of neuronal loss in the CA3 subregion of the hippocampus and inhibited the formation of aberrant Mossy Fiber Sprouting (MFS) (P<0.01). Furthermore, the ELISA data indicated a significant decrease in GFAP (P<0.01) and DNA fragmentation (P<0.05) following HGF administration. Conclusion: Our findings demonstrated the validity of HGF in protection against the progression of the kainate-induced TLE in rats. This measure improved learning, cognitive disturbances and inhibited apoptosis and astrogliosis. Highlights: Temporal lobe epilepsy results in apoptosis of neuronal cells;Hepatocyte growth factor attenuates the severity of status epilepticus in kainic acid-induced model;Hepatocyte growth factor attenuates apoptosis of neuronal cells in kainic acid-induced model of temporal lobe epilepsy. Plain Language Summary: Epilepsy is known as a disorder of the CNS which is caused by an imbalance in the electrical activity of neurons that in turn results in derangement in cognitive or causing debilitating seizures. Hepatocyte growth factor is one of neurotrophins secreted from mesenchymal and epithelial cells that regulate the growth, survival and functional changes of cells through signaling pathways such as the tyrosine kinase pathway after binding to its specific receptor. In this study, we tried to find out the effect of hepatocyte growth factor on attenuation of the severity of status epilepticus in kainic acid-induced model of temporal lobe epilepsy. Our results show that hepatocyte growth factor is able to protect against progression of the kainate-induced temporal lobe epilepsy in rats by improvement of learning, cognitive disturbances and inhibiting of apoptosis and astrogliosis.

Indexed as

ApoptosisAstrogliosisHepatocyte growth factorMemory impairmentTemporal lobe epilepsy

Identifiers

PMID35693152
PMCPMC9168821
OpenAlexW3212259105

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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.