AI Article Synopsis
- Epilepsy is common and serious, with research exploring the role of High-mobility Group Box 1 (HMGB1) and Toll-like Receptor 4 (TLR4) in seizures and their severity in animal models.
- A study involving 72 epilepsy patients found elevated serum levels of HMGB1 and TLR4, particularly higher in patients who are resistant to drug treatments versus those who respond to them.
- There was a significant correlation between HMGB1 and TLR4 levels, and HMGB1 was associated with seizure frequency, disease duration, and treatment response, suggesting they could be used as biomarkers for monitoring epilepsy treatment success.
Article Abstract
Epilepsy is one of the most common neurological diseases with severe outcome. High-mobility Group Box 1/Toll-like Receptor 4 axis is proposed to participate in the epileptogenesis and correlate with seizure severity in animal models. To explore whether HMGB1 and TLR4 could serve as clinical biomarkers in epileptic patients, we recruited a total of 72 epilepsy patients and measured the serum level of HMGB1 and TLR4 by flow fluorescence technology and ELISA respectively. We found that the serum levels of HMGB1 and TLR4 were elevated in epileptic patients. The serum levels of HMGB1 and TLR4 were also significantly higher in drug-resistant group compared with drug-effective group. There was a positive linear correlation between HMGB1 and TLR4 in the study group (R2 = 0.479). The HMGB1 level was found to be related to seizures frequency (F = 6.71, P = 0.012), the duration of disease (F = 6.55, P = 0.013) and drug reactivity (F = 3.96, P = 0.024) in epileptic patients, while TLR4 level was related to seizures frequency (F = 4.68, P = 0.034) and drug reactivity (F = 3.80, P = 0.027). Our result provides experimental evidences that the expression of HMGB1 and TLR4 was correlated with clinical symptom in epileptic patients, which could be used as clinical biomarkers to monitor therapeutic effect.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.eplepsyres.2023.107138 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Dual alarmin-receptor-specific targeting peptide systems for treatment of sepsis.
Acta Pharm Sin B
December 2024
Department of Molecular and Life Science, Hanyang University, Ansan 15588, Republic of Korea.
The pathophysiology of sepsis is characterized by a systemic inflammatory response to infection; however, the cytokine blockade that targets a specific early inflammatory mediator, such as tumor necrosis factor, has shown disappointing results in clinical trials. During sepsis, excessive endotoxins are internalized into the cytoplasm of immune cells, resulting in dysregulated pyroptotic cell death, which induces the leakage of late mediator alarmins such as HMGB1 and PTX3. As late mediators of lethal sepsis, overwhelming amounts of alarmins bind to high-affinity TLR4/MD2 and low-affinity RAGE receptors, thereby amplifying inflammation during early-stage sepsis.
View Article and Find Full Text PDFSufentanil attenuates renal ischemia-reperfusion injury via the lncRNA KCNQ1OT1/miR-211-5p/HMGB1 axis.
Pathol Res Pract
December 2024
Department of Anesthesiology, Nantong Haimen People's Hospital, Nantong 226100, China. Electronic address:
Inflammation is one of the most significant pathological changes in ischemia-reperfusion injury (IRI). Sufentanil has protective effects on IRI by reducing inflammatory responses. This study aimed to investigate the protective effects and possible mechanisms of sufentanil on renal IRI (RIRI).
View Article and Find Full Text PDFInhibition of RIPK1-driven necroptosis ameliorates inflammatory hyperalgesia caused by lipopolysaccharide: involvement of TLR-, NLRP3-, and caspase-11-mediated signaling pathways.
Cell Mol Biol (Noisy-le-grand)
January 2025
Department of Pharmacology, Faculty of Pharmacy, Mersin University, Mersin, Türkiye.
Article Synopsis
- Recent research indicates that blocking the RIPK1/RIPK3/MLKL necrosome can help reduce inflammatory pain linked to conditions like demyelination in the central nervous system.
- This study tests necrostatin-1s (Nec-1s), a specific RIPK1 inhibitor, on LPS-induced inflammatory pain in male mice, assessing pain sensitivity through hot plate tests and examining related protein changes.
- Results show that Nec-1s not only prevents LPS-induced pain relief but also reverses the activation of key proteins and signals involved in inflammation and demyelination, suggesting that RIPK1 inhibitors could be a promising treatment for managing inflammatory pain.
CD4+ T helper 2 cell-macrophage crosstalk induces IL-24-mediated breast cancer suppression.
JCI Insight
January 2025
Center for Cancer Immunology and Cutaneous Biology Research Center, Department of Dermatology and Krantz Family Center for Cancer Research, Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
CD4+ T cells contribute to antitumor immunity and are implicated in the efficacy of cancer immunotherapies. In particular, CD4+ T helper 2 (Th2) cells were recently found to block spontaneous breast carcinogenesis. However, the antitumor potential of Th2 cells in targeting established breast cancer remains uncertain.
View Article and Find Full Text PDFPain in rheumatoid arthritis: Emerging role of high mobility group box 1 protein-HMGB1.
Life Sci
January 2025
Agroprocessing and Technology Division, CSIR-National Institute for Interdisciplinary Science and Technology, Thiruvananthapuram 695019, Kerala, India; Academy of Scientific and Innovative Research (AcSIR), Ghaziabad 201002, India. Electronic address:
Rheumatoid arthritis (RA) is a chronic inflammatory disease where pain, driven by both inflammatory and non-inflammatory processes, is a major concern for patients. This pain can persist even after joint inflammation subsides. High mobility group box-1 (HMGB1) is a non-histone-DNA binding protein located in the nucleus that plays a key role in processes such as DNA transcription, recombination, and replication.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!