Canine Toll Like Receptor2 ELISA kit
- Known as:
- Canine Toll Like Receptor2 Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- e08t0068
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Blue gene shanghai
- Gene target:
- Canine Toll Like Receptor2 ELISA kit
Related genes to: Canine Toll Like Receptor2 ELISA kit
- Gene:
- TLR4 NIH gene
- Name:
- toll like receptor 4
- Previous symbol:
- -
- Synonyms:
- hToll, CD284, TLR-4, ARMD10
- Chromosome:
- 9q33.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-06-25
- Date modifiied:
- 2016-01-21
Related products to: Canine Toll Like Receptor2 ELISA kit
Related articles to: Canine Toll Like Receptor2 ELISA kit
- This study aims to investigate the potential protective effects of Achyranthes bidentata polysaccharides (ABPS) against severe traumatic brain injury (sTBI) and to elucidate the underlying mechanisms. - Source: PubMed
Publication date: 2026/08/15
Fang JingWeiChen XuxiaXie GuangMinLi KaiLv JunYing - Pediatric obstructive sleep apnea-hypopnea syndrome (OSAHS) associated with allergic rhinitis is characterized by persistent airway inflammation, in which the TLR4-MyD88-NF-κB signaling pathway plays a central role. Targeting this pathway may provide an effective strategy for modulating inflammatory responses. In the present study, an integrated computational and experimental approach was employed to identify and validate potential modulators of MyD88 signaling. De novo ligand design was performed to generate initial candidates, followed by artificial intelligence (AI)-based fragmentation and optimization to improve binding affinity and drug-like properties. Molecular docking and molecular dynamics simulations were conducted to evaluate binding stability and interaction profiles. The most promising compound was synthesized and structurally characterized using standard analytical techniques. Biological evaluation was performed across multiple in vitro models, including epithelial (RPMI 2650), macrophage (RAW 264.7), and mast cell (HMC-1) systems. Functional assays demonstrated that the optimized compound maintained cell viability while significantly reducing intracellular reactive oxygen species (ROS) levels. Western blot and quantitative PCR analyses revealed downregulation of key signaling components, including TLR4, MyD88, IRAK4, TRAF6, and NF-κB. In addition, ELISA-based cytokine profiling showed reduced levels of pro-inflammatory (TNF-α, IL-6, IL-1β) and Th2 cytokines (IL-4, IL-5, IL-13). Collectively, the findings indicate that the AI-fragmented lead compound was associated with attenuation of the TLR4-MyD88-NF-κB signaling axis across multiple biological levels. While further in vivo validation is required, this study highlights the potential of integrating AI-assisted drug design with experimental validation for the development of targeted therapeutics in inflammatory airway disorders. - Source: PubMed
Publication date: 2026/08/08
Gao JunSha XiaolanWang RongFu Yuanyuan - Rheumatoid arthritis (RA) is a chronic immune-mediated disease in which persistent inflammation and oxidative stress contribute to progressive joint damage. This study evaluated the prophylactic effects of sabinene in complete Freund's adjuvant (CFA)-induced arthritis and explored potential molecular associations using integrated in vivo and computational approaches. Rats were allocated to vehicle control, arthritic control, piroxicam, or sabinene groups (15, 30, or 60 mg/kg; n = 6/group); sabinene was administered orally beginning 30 minutes before CFA injection and continued for 28 days. Paw swelling, hematological and biochemical parameters, inflammatory and oxidative-stress markers, and gene expression were assessed, followed by network pharmacology, enrichment analysis, and molecular docking. Sabinene dose-dependently attenuated CFA-induced paw swelling and body-weight loss and improved hematological, hepatic, renal, and inflammatory parameters. Treatment also enhanced antioxidant defenses and reduced lipid peroxidation, prostaglandin E₂, 5-lipoxygenase, and anti-cyclic citrullinated peptide antibody levels. Sabinene reduced messenger RNA expression of nuclear factor kappa B (NF-κB), toll-like receptor 4 (TLR4), NOD-like receptor family pyrin domain-containing 3 (NLRP3), caspase-1, gasdermin D, and other pro-inflammatory genes while increasing interleukin-4 and interleukin-10 expression. Network pharmacology identified 133 overlapping sabinene-RA targets, and molecular docking predicted interactions with tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), signal transducer and activator of transcription 3 (STAT3), and interferon gamma (IFN-γ). These findings support a prophylactic protective effect of sabinene against CFA-induced arthritis associated with reduced inflammation, improved antioxidant status, and modulation of inflammasome-related gene expression. Further protein-level, functional, and post-induction studies are required to confirm the proposed mechanisms and therapeutic relevance. - Source: PubMed
Publication date: 2026/08/14
Asif KanwalUttra Ambreen MalikShabbir ArhamQasim SumeraKalsoom SaimaAlhazza AbdulelahAlotaibi HamoudAl Hamod MonaAlfuraih SalehAlmutairy Ali FAlharbi Raiyan FaisalAhmad Ashfaq - Efferocytosis, the phagocytic clearance of dying cells, by microglia is crucial for limiting neuroinflammation and promoting resolution in ischemic stroke. Extracellular cold-inducible RNA-binding protein (eCIRP) is an inflammatory mediator that impairs macrophage bacterial phagocytosis in sepsis and radiation injury, but its role in microglial efferocytosis in ischemic stroke has not yet been studied. Using a transient middle cerebral artery occlusion (tMCAO) model of ischemic stroke, this study demonstrated that eCIRP is released into the cerebrospinal fluid and microglial expression of the crucial efferocytic receptor MerTK decreases in tMCAO mice. CIRP deficiency significantly improved MerTK expression and microglial efferocytosis in tMCAO mice, reducing brain infarction, inflammation, neurological deficit, and survival in acute stroke. eCIRP induces pro-inflammatory micro-RNA 155 (miR-155) via TLR4, which suppresses its target pro-efferocytic transcription factor MAF bZIP (MafB), downregulating MerTK and the downstream cytoskeletal regulators, to impair microglial efferocytosis. Pharmacological blockade of eCIRP-TLR4 interaction using small peptide C23 attenuates miR-155 induction, restores MerTK expression, rescues microglial efferocytosis, and improves outcomes in tMCAO mice. This study uncovers a previously unknown pathway through which eCIRP signaling impairs neuroprotective efferocytic microglial function in ischemic stroke, suggesting that targeting eCIRP may promote functional recovery after stroke. - Source: PubMed
Publication date: 2026/08/15
Lapin DmitriyAylar DilaraSharma ArchnaWang Ping - Adverse outcome pathways (AOPs) describe toxicity across levels of biological organization by measurable key events (KEs), thus providing a structured framework for predicting population-level effects. Here, mussels were exposed to different temperature conditions-22 °C and marine heatwave (MHW), in combination with nano-titanium dioxide (nano-TiO) at 0, 25, and 250 μg/L. High-concentration nano-TiO and MHW exposure promoted the secretion of byssal threads and enhanced the adhesion to the substrate. However, they also caused severe histopathological damage in the foot and reduced the condition index (CI), indicating serious organism-level adverse outcomes (AOs). Accumulation of lipid peroxidation (LPO) products and redox imbalance suggested that MHW and nano-TiO induced oxidative stress, leading to increased cell apoptosis (CA), reduced cell viability (CV), and consequent tissue damage in the foot. Nano-TiO and MHW exposure significantly upregulated adhesion-related genes () as well as immune- and cytotoxicity-related genes (, , , and ). In contrast, and pre-collagen proteins () were significantly downregulated, resulting in poor extensibility of byssal threads. Using the AOP framework, this study links nano-TiO toxicity and MHW-induced stress to molecular disruptions, organism-level adverse outcomes, and altered mussel byssal defenses. These findings highlight that the interaction between MHW and nanoparticles may compromise mussel attachment and survival, with potential implications for the stability of coastal benthic ecosystems under future climate change scenarios. - Source: PubMed
Publication date: 2026/07/17
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