ArticleMolecular medicine reports2017
HMGB1 regulates P-glycoprotein expression in status epilepticus rat brains via the RAGE/NF-κB signaling pathway.
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 19 papers.
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.
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.
Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Pathophysiology of Status Epilepticus Revisited.International journal of molecular sciences · 2025Review
- Seizures in brain tumors: pathogenesis, risk factors and management (Review).International journal of molecular medicine · 2025Review
- Small-molecule caspase-1 inhibitor CZL80 terminates refractory status epilepticus via inhibition of glutamatergic transmission.Acta pharmacologica Sinica · 2024Article
- Advances in the Study of Non-Coding RNA in the Signaling Pathway of Pulmonary Fibrosis.International journal of general medicine · 2024Review
- Insight into Drug Resistance in Status Epilepticus: Evidence from Animal Models.International journal of molecular sciences · 2023Review
- The effect of olsalazine of chinese generic drugs on ulcerative colitis induced by dextran sulfate sodium salt in BALB/c mice.Acta cirurgica brasileira · 2023Article
- Astrocytes as a target for therapeutic strategies in epilepsy: current insights.Frontiers in molecular neuroscience · 2023Review
- Review and prospect of immune checkpoint blockade therapy represented by PD-1/PD-L1 in the treatment of clear cell renal cell carcinoma.Oncology research · 2023Review
- Transporter Regulation in Critical Protective Barriers: Focus on Brain and Placenta.Pharmaceutics · 2022Review
- Comparison of the cardiovascular system, clinical condition, and laboratory results in COVID-19 patients with and without vitamin D insufficiency.BMC infectious diseases · 2022Article
- Paeonol Protects Against Methotrexate-Induced NephrotoxicityFrontiers in pharmacology · 2022Article
- Anti-high mobility group box protein 1 monoclonal antibody downregulating P-glycoprotein as novel epilepsy therapeutics.The Egyptian journal of neurology, psychiatry and neurosurgery · 2022Review
- Blocking receptor for advanced glycation end products (RAGE) or toll-like receptor 4 (TLR4) prevents posttraumatic epileptogenesis in mice.Epilepsia · 2021Article
- Review
- Ibuprofen Exerts Antiepileptic and Neuroprotective Effects in the Rat Model of Pentylenetetrazol-Induced Epilepsy via the COX-2/NLRP3/IL-18 Pathway.Neurochemical research · 2020Article
- Advanced Glycation End Products and Receptor (RAGE) Promote Wound Healing of Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2020Article
- Molecular alterations of the TLR4-signaling cascade in canine epilepsy.BMC veterinary research · 2020Article
- Knockdown of long non‑coding RNA PVT1 reverses multidrug resistance in colorectal cancer cells.Molecular medicine reports · 2018Article
- HMGB1: A Common Biomarker and Potential Target for TBI, Neuroinflammation, Epilepsy, and Cognitive Dysfunction.Frontiers in neuroscience · 2018Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of P-glycoprotein (P-gp) in the brain is an important mechanism involved in drug‑resistant epilepsy (DRE). High-mobility group box 1 (HMGB1), an inflammatory cytokine, significantly increases following seizures and may be involved in upregulation of P‑gp. However, the underlying mechanisms remain elusive. The aim of the present study was to evaluate the role of HMGB1 and its downstream signaling components, receptor for advanced glycation end‑product (RAGE) and nuclear factor‑κB (NF‑κB), on P‑gp expression in rat brains during status epilepticus (SE). Small interfering RNA (siRNA) was administered to rats prior to induction of SE by pilocarpine, to block transcription of the genes encoding HMGB1 and RAGE, respectively. An inhibitor of NF‑κB, pyrrolidinedithiocarbamic acid (PDTC), was utilized to inhibit activation of NF‑κB. The expression levels of HMGB1, RAGE, phosphorylated‑NF‑κB p65 (p‑p65) and P‑gp were detected by western blotting. The relative mRNA expression levels of the genes encoding these proteins were measured using reverse transcription‑quantitative polymerase chain reaction and the cellular localization of the proteins was determined by immunofluorescence. Pre‑treatment with HMGB1 siRNA reduced the expression levels of RAGE, p‑p65 and P‑gp. PDTC reduced the expression levels of P‑gp. These findings suggested that overexpression of P‑gp during seizures may be regulated by HMGB1 via the RAGE/NF‑κB signaling pathway, and may be a novel target for treating DRE.
Indexed as
Identifiers
What 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.