Bovine Interleukin 6,IL-6 ELISA Kit
- Known as:
- Bovine Interleukin 6,Interleukin-6 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0000BO
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Bovine Interleukin 6 IL-6 ELISA Kit
Related genes to: Bovine Interleukin 6,IL-6 ELISA Kit
- Gene:
- CEBPB NIH gene
- Name:
- CCAAT enhancer binding protein beta
- Previous symbol:
- TCF5
- Synonyms:
- LAP, CRP2, NFIL6, IL6DBP, C/EBP-beta
- Chromosome:
- 20q13.13
- Locus Type:
- gene with protein product
- Date approved:
- 1991-02-27
- Date modifiied:
- 2018-02-23
- Gene:
- CEBPD NIH gene
- Name:
- CCAAT enhancer binding protein delta
- Previous symbol:
- -
- Synonyms:
- CRP3, CELF, C/EBP-delta, NF-IL6-beta
- Chromosome:
- 8q11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1992-06-24
- Date modifiied:
- 2018-02-23
- Gene:
- ENTPD6 NIH gene
- Name:
- ectonucleoside triphosphate diphosphohydrolase 6
- Previous symbol:
- CD39L2, IL6ST2
- Synonyms:
- NTPDase-6, dJ738P15.3
- Chromosome:
- 20p11.21
- Locus Type:
- gene with protein product
- Date approved:
- 1998-03-20
- Date modifiied:
- 2019-02-28
- Gene:
- IL6 NIH gene
- Name:
- interleukin 6
- Previous symbol:
- IFNB2
- Synonyms:
- IL-6, BSF2, HGF, HSF
- Chromosome:
- 7p15.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2017-07-12
- Gene:
- IL6RP1 NIH gene
- Name:
- interleukin 6 receptor pseudogene 1
- Previous symbol:
- IL6RL1
- Synonyms:
- -
- Chromosome:
- 9q22.2
- Locus Type:
- pseudogene
- Date approved:
- 1991-08-18
- Date modifiied:
- 2014-11-19
Related products to: Bovine Interleukin 6,IL-6 ELISA Kit
Related articles to: Bovine Interleukin 6,IL-6 ELISA Kit
- The etiology of pediatric autism spectrum disorder (ASD) has been increasingly linked to alterations in the gut-brain axis, highlighting the intricate bidirectional communication between gut microbiota and central nervous system. The molecular mechanisms of this communication are poorly understood. Here we investigated whether ASD-associated gut microbiota could exhibit altered inflammatory molecular outputs by integrating chemistry-driven profiling of fecal lipopolysaccharides (LPS), functional bacterial proteomics, and neuroimmune cellular assays. Structural analyses revealed that LPS from non-autistic healthy donors (NASD) displayed highly conserved carbohydrate and lipid A signatures dominated by hypo-acylated mono-phosphorylated species typically associated with immunomodulatory Bacteroides-derived LPS. In contrast, LPS from ASD children exhibited increased structural heterogeneity. These molecular alterations were functionally reflected in human HMC3 microglial cells, where ASD-derived fecal LPS induced stronger IL-6 and IL-8 release compared with NASD-derived LPS, indicating enhanced neuroinflammatory potential. Functional proteomic profiling disclosed broadly comparable microbial compositions but marked metabolic divergence. These findings suggest that gut microbiota in ASD children are associated with a functionally heterogeneous microbial ecosystem characterized by altered immunostimulatory molecular outputs despite the absence of massive taxonomic shifts, with potential relevance for neuroimmune dysregulation. - Source: PubMed
De Chiara StefaniaDi Somma AngelaMazziotti ValentinaCoppola SerenaOglio FrancaTammaro LidiaRiccio Maria PiaBravaccio CarmelaMolinaro AntonioBerni Canani RobertoDi Lorenzo Flaviana - Cardiac surgery-associated acute kidney injury (CSA-AKI) occurs in 20-30% of patients after heart surgery with cardiopulmonary bypass (CPB). AKI rates are even higher in VA ECMO treated patients. The pathogenesis of CSA-AKI is incompletely understood, and preventative therapies are lacking. We hypothesize that CSA-AKI occurs due to pump related RBC hemolysis and accumulation of cell-free hemoglobin (CFH) and hemopexin in the kidneys. - Source: PubMed
Publication date: 2026/09/29
Smedlund KathrynBekbolsynov DulatAzizi MustafaLad ApurvaManandhar SareetaGunning William TJansen Sebastian VStrudthoff Lasse JLeaf David EStepkowski StanislawGupta Rajesh - Atherosclerosis is a chronic inflammatory disease in which oxidative stress serves as a final common mechanism linking endothelial injury, lipoprotein oxidation, immune activation, and plaque progression. Since the original description of reactive oxygen species (ROS) generating and antioxidant systems in atherogenesis, substantial advances have reshaped the mechanistic and therapeutic landscape. This review provides a comprehensive update on oxidative stress in atherosclerosis, with particular emphasis on the LOX-1-NLRP3 inflammasome axis as a central driver of residual inflammatory risk. - Source: PubMed
Publication date: 2026/09/29
Garg KeshavGautam NiteshAgrawal AnkitMehta Jawahar L - Mechanical ventilation is associated with acute and long-term cognitive dysfunction, yet the molecular pathways linking ventilator-induced lung injury (VILI) to brain injury remain poorly characterized. We previously demonstrated that peripheral IL-6 signaling mediates delirium-like phenotypes in a murine VILI model. Here, we use unbiased aptamer-based proteomics to determine whether this model exhibits proteomic signatures consistent with neurodegenerative processes in the brain and plasma. - Source: PubMed
Publication date: 2026/09/29
Winzey Kevin DGuzman SamuelYang EdwardMoreira DebbieWang XingyuGu XuesongDillon Simon TEly E WesleyKarumanchi S AnanthLibermann Towia ALahiri Shouri - Alzheimer's disease (AD) and periodontitis (PD) are highly prevalent chronic disorders in ageing populations and share multiple pathological features, particularly persistent inflammatory and immune dysregulation. Despite increasing evidence supporting an association between the two diseases, the shared druggable molecular mechanisms underlying their comorbidity remain incompletely understood, and effective therapeutic strategies capable of simultaneously targeting shared disease-related processes are limited. This study aimed to identify shared druggable molecular candidates associated with AD and PD and to evaluate the potential biological effects of the natural products amentoflavone (AF) and taraxerone (TA) in AD-PD-related inflammatory cell models. An integrative strategy combining Mendelian randomisation (MR), transcriptomic profiling, machine learning, and structure-based virtual screening was used to identify and prioritise shared molecular candidates associated with AD and PD. Molecular docking and molecular dynamics (MD) simulations were performed to evaluate the predicted binding modes and interaction stability of AF and TA with selected core proteins. In vitro experiments were conducted using LPS-induced mouse BV2 microglia and mouse primary gingival fibroblasts (MGFs) to assess the effects of AF and TA, alone and in combination, on core-gene expression, inflammatory mediator secretion, oxidative stress, apoptosis, and iNOS/CD206-defined microglial activation states. MR, transcriptomic, and machine-learning analyses prioritised six shared key genes, including FCGRT, LTBP1, CD59, SPRED1, SURF2, and ZDHHC2, with FCGRT, SPRED1, and SURF2 selected for subsequent structural and cellular investigations. Molecular docking and MD simulations suggested stable predicted interactions of AF and TA with these three proteins. AF formed persistent hydrogen-bond networks, particularly in the SPRED1 and SURF2 complexes, whereas TA interactions were predominantly hydrophobic. MM-PBSA analysis yielded favourable binding free energies ranging from - 62.4 to - 99.7 kJ/mol. AF at 10 µM and TA at 20 µM were selected as non-cytotoxic working concentrations for subsequent cellular experiments. Both compounds partially restored LPS-associated alterations in FCGRT, SPRED1, and SURF2 expression, reduced TNF-α, IL-1β, and IL-6 secretion, increased IL-10 production, attenuated oxidative stress by reducing ROS, MDA, and NO levels while increasing SOD activity, decreased apoptosis, and shifted the iNOS/CD206-defined microglial activation profile away from an LPS-induced pro-inflammatory state toward an anti-inflammatory or repair-associated response. AF + TA co-treatment produced greater combined effects than either single treatment in several assays; however, quantitative combination analyses are required to determine whether these effects represent pharmacological synergy or additive interactions. This study identified FCGRT, SPRED1, and SURF2 as prioritised shared molecular candidates associated with AD and PD and provided computational and cellular evidence supporting further investigation of AF and TA as potential natural-product-based therapeutic candidates. AF and TA showed stable predicted interactions with the selected proteins and modulated gene-expression, inflammatory, oxidative-stress, apoptotic, and microglial-activation-related phenotypes in LPS-induced cellular models. These findings provide additional insight into the shared molecular landscape of AD and PD and support further experimental evaluation of AF and TA, including direct target-engagement studies, quantitative combination analyses, and in vivo validation. - Source: PubMed
Publication date: 2026/09/29
Wu YekeLi ShuangZhang XimeiXu QianrongChen BingjunYang WenbinLiu MinLi JiaweiHe XiangLi JuanWu Wenbin