IL-18 BP, Human Protein
- Known as:
- Interleukin-18 BP, Human Protein
- Catalog number:
- z03168-50
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- IL-18 Human Protein
Related genes to: IL-18 BP, Human Protein
- 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: IL-18 BP, Human Protein
Related articles to: IL-18 BP, Human Protein
- Radiation-induced intestinal injury (RIII) is a common complication of radiotherapy for abdominal and pelvic malignancies, for which effective therapeutic options remain limited. Baicalin, a flavonoid derived from Scutellaria baicalensis, exhibits anti-inflammatory and antioxidant properties, but its role in RIII and underlying mechanisms remain unclear. C57BL/6J mice were exposed to total body irradiation (8.5 Gy) and treated with baicalin (25, 50, or 100 mg/kg/d) for 10 consecutive days. Intestinal injury was evaluated by histology, colon length, tight junction protein expression, and inflammatory cytokine levels. Ferroptosis was assessed by measuring glutathione peroxidase 4 (GPX4) expression and oxidative stress markers (MDA, GSH/GSSG). Human NCM460 colon epithelial cells were exposed to 10 Gy irradiation with or without baicalin (20 µM) to evaluate cell viability, invasion, apoptosis, GPX4 expression, Fe²⁺ accumulation, and reactive oxygen species (ROS) production. Baicalin treatment dose-dependently improved survival, increased food intake, attenuated body weight loss, and restored fecal output in irradiated mice. Baicalin alleviated intestinal histopathological damage, preserved colon length, restored ZO-1 and occludin expression, and suppressed IL-1β, IL-18, and TNF-α release. Notably, baicalin ameliorated radiation-induced mitochondrial damage, upregulated GPX4 expression, reduced MDA and GSSG levels, and restored GSH levels. In vitro, baicalin enhanced cell viability and proliferation, restored invasion capacity, and reduced apoptosis in irradiated NCM460 cells. Mechanistically, baicalin upregulated GPX4 expression and suppressed radiation-induced Fe²⁺ accumulation and ROS generation without affecting acyl-CoA synthetase long-chain family member 4 (ACSL4) expression. Baicalin protects against radiation-induced intestinal injury by inhibiting GPX4-mediated ferroptosis, suggesting its potential as a therapeutic agent for RIII. - Source: PubMed
Publication date: 2026/07/20
Huang JieXia JinlinShao Na - Qi Huang Granules (QHG), a traditional Chinese medicine (TCM) formulation, have been applied clinically for over two decades to treat dry age-related macular degeneration (AMD) and associated fundus lesions. Although its retinoprotective effects have been documented, the associated underlying mechanisms are largely unexplored. The present work focused on investigating the therapeutic efficacy of QHG in sodium iodate (NaIO₃)-induced retinal damage, with a particular focus on how the formula regulated the interaction between inflammatory responses and imbalances in mitochondrial dynamics. UPLC-HRMS, network pharmacology, and molecular docking analyses were integrated for identifying mitochondria-associated bioactive constituents and potential targets of QHG. In the experimental model, retinal injury was induced in rats through tail vein injection of NaIO. Retinal morphological and ultrastructural changes were assessed by HE staining and transmission electron microscopy. To assess mitochondrial function, mitochondrial membrane potential, mtROS levels, and mtDNA integrity were measured. Additionally, ELISA was performed to quantify IL-1β and IL-18 levels. Key marker levels, including p-DRP1, DRP1, OPA1, MFN2, and NLRP3, were determined by Western blotting, IHC, and qRT-PCR. DNM1L (encoding DRP1) and MFN2 were identified as the primary targets of QHG through UPLC-HRMS and computational analyses. In vivo experimental results showed that treatment with QHG alleviated morphological alterations and ultrastructural damage to the retina and mitochondria in model rats. Furthermore, QHG treatment increased mitochondrial membrane potential, reduced mtROS levels, mitigated mtDNA damage, and reduced IL-1β and IL-18 contents. Mechanistically, QHG downregulated p-DRP1, DRP1, and NLRP3, while upregulating MFN2 and OPA1. Collectively, these findings demonstrate that QHG can ameliorate retinal morphology and ultrastructural damage in mitochondria, such as cellular mitochondria, improve mitochondrial function, and attenuate retinal inflammation, thereby exerting a protective effect against NaIO₃-induced retinal injury. The underlying mechanism may involve the mitochondrial dynamics-NLRP3 pathway. - Source: PubMed
Publication date: 2026/07/20
Wang JifangWu ZhiqiangFang LuluGuo YuxinLi HongmeiLiang Fengming - To investigate evidence of central nervous system (CNS) injury in Post-COVID-19 Condition (PCC) through plasma biomarkers of neuronal damage (APP, NfL, Tau), inflammation (IL-2, IL-6, IL-10, IL-18, IFN-γ, TNF-α), and immune response (IgM, IgA, IgG) in individuals with PCC and neurological symptoms. - Source: PubMed
Publication date: 2026/07/14
de Souza Fonseca Grazielede Mello Carpes RaphaelPereira Marcela Espindola Palmeirade Barros Cintia Monteiro - Osteoarthritis (OA) is a prevalent degenerative joint disease characterized by progressive cartilage destruction. Emerging evidence suggests that chondrocyte pyroptosis, a pro-inflammatory programmed cell death pathway, contributes to OA pathogenesis. However, the molecular mechanisms underlying pyroptosis in OA and potential therapeutic interventions remain incompletely understood. Bulk RNA-seq datasets (GSE114007 and GSE254844) were analyzed to identify differentially expressed genes (DEGs) and co-expression modules via DESeq2 and WGCNA. Shared key DEGs (SKDEGs) were subjected to GO and KEGG enrichment analyses to reveal relevant pathways. Pyroptosis-related DEGs (PRDEGs) were intersected with SKDEGs and used for drug prediction in EnrichR. Predicted compounds were further examined for potential targets using TCMSP, HIT, and SwissTargetPrediction databases to identify hub genes. Single-cell RNA-seq data (GSE169454) were analyzed to determine the cellular localization, differential expression, and pathway activity of hub genes. Finally, in vitro experiments with primary human normal and OA chondrocytes were performed to validate the effects of the identified compound on cell proliferation and pyroptosis. Analysis of bulk RNA-seq data identified 146 SKDEGs, with pyroptosis emerging as the most significantly enriched pathway. Six PRDEGs were identified, and curcumin was predicted as a key therapeutic compound. Intersection of curcumin targets with PRDEGs revealed four hub genes (CASP1, IL1B, IL18, NLRP3), all upregulated in OA. Single-cell analysis confirmed that these hub genes were predominantly expressed in OA-associated chondrocyte subtypes, with increased pathway activity and expression along pseudotime trajectories. In vitro, curcumin (10 µM) promoted chondrocyte proliferation and significantly suppressed the mRNA and protein expression of the hub genes, indicating inhibition of pyroptosis. Chondrocyte pyroptosis is a critical contributor to OA progression, and curcumin can alleviate OA by targeting pyroptosis-related pathways. This integrative study provides mechanistic insights and a potential therapeutic strategy for OA. - Source: PubMed
Publication date: 2026/07/20
Huang JuanZhang ChiHe QingchuanChen YuanChen RuyanYang Shibin - The objective of this study is to explore the expression patterns of angiogenesis-related genes in papillary thyroid cancer (PTC) to enhance understanding of the molecular mechanisms underlying angiogenesis in this malignancy. The findings provide valuable insights into the development of therapeutic strategies. - Source: PubMed
Publication date: 2026/07/19
Zhao JunQin Ya-XinZhao MinNiu HuiLiu Xiao-Qi