ArticleBioengineered2022
Long non-coding RNA H19 alleviates hippocampal damage in convulsive status epilepticus rats through the nuclear factor-kappaB signaling pathway.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Evaluating long non-coding RNA signatures as biomarkers for inflammatory pathway regulation and rehabilitative outcomes in Parkinson's disease: toward a precision medicine approach.Frontiers in immunology · 2026Article
- Silencing epileptic storms: targeting miRNA-lncRNA crosstalk in astrocytes and microglia to disarm neuroinflammatory triggers.Frontiers in molecular neuroscience · 2025Review
- Identification and coregulation pattern analysis of long noncoding RNAs in the mouse brain after Angiostrongylus cantonensis infection.Parasites & vectors · 2024Article
- The regulatory function of lncRNA and constructed network in epilepsy.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2023Review
- Immunological Imbalances Associated with Epileptic Seizures in Type 2 Diabetes Mellitus.Brain sciences · 2023Review
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have demonstrated that inflammation plays a critical role in hippocampcal damage and cognitive dysfunction induced by convulsive status epilepticus (CSE). Emerging evidence indicated that the long non-coding RNA (lncRNA) H19 acts as an important regulator of inflammation in various diseases. However, the role of H19 in CSE is still unkonwn. In the present study, pilocarpine-induced SE rat model was used to explore the role of H19 in hippocampal neuron damage in CSE. Our results indicated that the increased level of H19 is positively correlated with the expression of inflammatory cytokines (TNF-α and IL-1β) in hippocampus of SE rats. Moreover, knockdown of H19 could inhibit the activation of microglia and suppress the expression of inflammatory cytokines via nuclear factor-kappaB (NF-κB) signaling pathway. It was further revealed that downregulation of H19 could alleviate hippocampal neuron damage induced by CSE. These findings indicated that H19 modulates inflammatory response and hippocampal damage through the NF-κB signaling pathway in the CSE rats, which provides a promising target to alleviate hippocampcal damage of CSE.
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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 Socratic graph.