Human IL-18 ELISA kit
- Known as:
- Human Interleukin-18 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1125
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Human IL-18 ELISA kit
Related genes to: Human IL-18 ELISA kit
- Gene:
- IL18 NIH gene
- Name:
- interleukin 18
- Previous symbol:
- -
- Synonyms:
- IGIF, IL1F4, IL-1g, IL-18
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1997-07-25
- Date modifiied:
- 2015-07-06
- Gene:
- IL18BP NIH gene
- Name:
- interleukin 18 binding protein
- Previous symbol:
- -
- Synonyms:
- IL18BPa
- Chromosome:
- 11q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-21
- Date modifiied:
- 2016-10-05
Related products to: Human IL-18 ELISA kit
Related articles to: Human IL-18 ELISA kit
- The hallmarks of Alzheimer's disease (AD), a progressive neurodegenerative disease, include tau tangles, amyloid-β (Aβ) plaques, cognitive impairment, and severe neuroinflammation. A key molecular mediator linking immunological activation and neurological pathology in AD is the NLRP3 inflammasome. This review explains the intricate role of the NLRP3 inflammasome in AD, including its structure, activation mechanisms, and regulatory signaling pathways. The pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) that activate NLRP3 include oxidative stress, Aβ, mitochondrial dysfunction, ion fluxes, gut dysbiosis, and mitochondrial malfunction. Pro-inflammatory cytokines IL-1β and IL-18 are released when the inflammasome assembles with ASC and procaspase-1, leading to caspase-1 activation and pyroptosis. The article investigates both canonical and noncanonical pyroptosis pathways and provides detailed insights into how glial cells-specifically microglia and astrocytes-are involved in NLRP3-mediated neuroinflammation. It has been demonstrated that NLRP3 activation is modulated by several receptor-mediated signaling pathways, including NF-κB, TLR4, TREM2, purinergic, and MAP4K6, which intensify inflammatory responses in the AD brain. Furthermore, the review assesses preclinical and clinical research targeting NLRP3 and its upstream regulators, emphasizing potential treatment options as Simufilam, MCC950, OLT1177, and CY-09. This work highlights the therapeutic potential of the inflammasome and promotes the development of targeted anti-inflammatory treatments to ameliorate AD pathology by elucidating the molecular mechanisms linking NLRP3 to AD progression. - Source: PubMed
Publication date: 2026/06/02
Chaudhary BharatKumari SnehaSharma PrajjwalDhapola RishikaPaidlewar MohitVellingiri BalachandarMedhi BikashHariKrishnaReddy Dibbanti - This study aimed to develop a robust predictive model and nomogram for breast cancer (BC) based on genes associated with diverse cell death methods. A prognostic model was constructed using the LASSO Cox method, incorporating twelve genes (CREB3L1, SFRP1, SHARPIN, AIFM1, IL‑18, CD24, EDA2R, CRIP1, XBP1, BCL2A1, NKX3‑1, and NME5). BC patients were classified into high‑risk and low‑risk subgroups, with the low‑risk subgroup showing superior survival, and this prognostic value was validated in an independent external cohort. A nomogram was also developed and confirmed as a reliable independent predictor of outcome. Enrichment analyses suggested a link between patient risk and immune response. The low‑risk subgroup exhibited a higher tumor microenvironment (TME) score. Patients in the high‑risk group showed improved responses to lapatinib, BI‑2536, OSI‑027, and SB505124, whereas those in the low‑risk subgroup had better sensitivity to axitinib, epirubicin, fulvestrant, and olaparib. Additionally, CD24 overexpression in BC cell lines promoted proliferation and migration, and inhibited apoptosis. These findings contribute to personalized treatment strategies and help elucidate the tumor microenvironment characteristics of BC patients. - Source: PubMed
Wu RihanWang ZiruiBai YuanruiDong ChunhuiLiu YihuiChen Ling - 2-Ethylhexyl diphenyl phosphate (EHDPHP) is a widely used organophosphorus flame retardant frequently detected in environmental matrices and poses potential health risks. However, its cardiotoxic effects on mammalian cardiomyocytes and the underlying molecular mechanisms remain largely unclear. Niacin (NIA), an essential water-soluble vitamin, exhibits potent antioxidant, anti-inflammatory, and mitochondrial-protective activities. In this study, we investigated EHDPHP-induced toxicity in H9C2 cardiomyocytes and the protective effects of NIA. Cells were exposed to 100 μM EHDPHP alone or in combination with 400, 600, and 800 μM NIA. EHDPHP exposure significantly reduced cell viability, disrupted the balance between pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, and IL-18) and the anti-inflammatory cytokine IL-10, and induced oxidative stress, as evidenced by elevated ROS, MitoSOX, and MDA levels alongside decreased activities of antioxidant enzymes (SOD, GSH, GSH-Px, and CAT). Additionally, EHDPHP disturbed mitochondrial dynamics by promoting fission and inhibiting fusion, impaired mitochondrial biogenesis via downregulation of AMPK and PGC-1α, triggered excessive mitophagy through PINK1, PRKN, and LC3 upregulation, and activated pyroptosis via GSDMD, NLRP3, and Caspase-1. Bioinformatics analyses confirmed the interconnected regulatory network among mitochondrial dynamics, mitophagy, pyroptosis, and inflammatory signaling in EHDPHP-induced cardiomyocyte injury. Notably, NIA intervention dose-dependently mitigated these detrimental effects, restoring cell viability, alleviating inflammation and oxidative stress, rebalancing mitochondrial fusion and fission, rescuing biogenesis, normalizing mitophagy, and inhibiting pyroptosis. These findings reveal a pathological cascade through which EHDPHP induces cardiomyocyte injury and demonstrate that NIA confers cardioprotection by targeting multiple pathological pathways. This study provides novel mechanistic insights into EHDPHP-induced cardiotoxicity and highlights NIA as a promising nutritional intervention for reducing cardiovascular risks associated with environmental pollutants. - Source: PubMed
Dai LizhiWang JingxuanLiu JiaCao ZheyuanZhang YuhaoLi YouchongYu TongXiao Jianhua - This study evaluated the therapeutic effectiveness and safety of tocilizumab (TCZ) in patients with systemic juvenile idiopathic arthritis (sJIA)-associated refractory macrophage activation syndrome (MAS). A total of 100 patients diagnosed between 2021 and 2022 were included. Patients receiving standard therapy (glucocorticoids plus cyclosporine A) were assigned to the control group (n = 30), while those receiving add-on TCZ were assigned to the study group (n = 70). The treatment protocol included intravenous methylprednisolone pulses followed by oral prednisone tapering, cyclosporine A with trough monitoring, and TCZ administered every 2 weeks. Outcomes included laboratory parameters, cytokine profiles (IL-6, IL-18, IFN-γ, sCD25, sCD163), sJADAS27 scores, clinical response, and adverse events over 24 months. The TCZ group demonstrated faster normalization of laboratory indices and greater reduction in inflammatory cytokines (P < 0.05). Remission rates were higher (71.4% vs. 33.3% at Day 14), with lower recurrence and reduced glucocorticoid exposure. Adverse event rates were lower in the TCZ group (25.7% vs. 46.7%, P < 0.05). These findings demonstrate that TCZ-based combination therapy provides an effective and well-tolerated salvage strategy for refractory sJIA-MAS and support further prospective evaluation of this protocol. - Source: PubMed
Publication date: 2026/05/15
Wang XuepingAn Yan - Gonorrhoea, a common sexually transmitted disease, is caused by . The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome regulates interleukin (IL)-1β and IL-18 secretion via caspase-1 activation and plays a critical role in inflammation. Dysregulation of the NLRP3 inflammasome contributes to various diseases, making it a promising therapeutic target. We previously showed that activates the NLRP3 inflammasome in macrophages. This study aimed to explore the anti-inflammatory potential of cinnamaldehyde (CA), the major aldehyde in Kaneh essential oil, in -infected macrophages. - Source: PubMed
Publication date: 2025/06/25
Hua Kuo-FengChiu Hsiao-WenChen Miao-MeiWong Wei-TingTsai Wen-ChiuanLin Wen-YuWu Chun-HsienWang Chien-ChunHsu Chung-HuaChernikov Oleg VRao Yerra KoteswaraHsu Hsien-TaHo Chen-LungLi Lan-Hui