Canine Interleukin 6,IL-6 ELISA Kit
- Known as:
- Canine Interleukin 6,Interleukin-6 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0003Ca
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Canine Interleukin 6 IL-6 ELISA Kit
Related genes to: Canine 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: Canine Interleukin 6,IL-6 ELISA Kit
Related articles to: Canine Interleukin 6,IL-6 ELISA Kit
- Colorectal cancer (CRC) is still one of the main reasons for death from cancer worldwide. Xian Lian Jie Du decoction (XLJD) is based on Professor Zhou Zhongying's idea of "tumour toxins", and it has shown some therapeutic effects in CRC; however, its active ingredients and specific molecular targets are not yet fully known. Active constituents of XLJD were screened from the TCMSP database (oral bioavailability ≥30%, drug-likeness ≥0.18). Predicted targets were cross-referenced with CRC-related genes from GeneCards, OMIM, and TTD, and a protein-protein interaction network was built to identify hub targets, which were then annotated using GO and KEGG enrichment. Quercetin, Kaempferol, Luteolin and some other compounds were chosen for molecular docking and 100-ns molecular dynamics simulations. LC-MS was used to identify the XLJD formulation, and then CCK-8 assays and RT-qPCR were carried out to determine the changes in gene expression in HT-29 cells. A total of 197 shared targets were found in XLJD and CRC. Topological evaluation shows that HIF1A, IL6, JUN, MMP9 and TNF are important genes, and most of them belong to the TNF, IL-17 and AGE-RAGE signalling pathways. All fifteen ligand-protein complexes had a docking energy below (more negative than) -5.0 kcal/mol, and TNF was one of them; Molecular dynamics also showed that it had a good binding affinity and formed continuous hydrogen bonds and a stable low-energy state. LC-MS was used to identify the three kinds of compounds: quercetin, hesperidin and luteolin. A large amount of XLJD and every three flavonoids significantly reduced the mRNA expression of the five hub genes in HT-29 cells; however, the low-concentration group had little to no effect. In summary, XLJD and some of its main flavonoids may be targeting a group of CRC-related genes that are controlled by HIF1A, IL6, JUN, MMP9, TNF, etc. The above are the first transcriptional data; protein-based and verification will still be needed. - Source: PubMed
Publication date: 2026/08/31
Du NingJi LiLiu LixingLiu XinqiJiang ZhenglongYin YukunFeng Li - Neuroinflammation following acute cerebral infarction (ACI) critically contributes to disease pathophysiology, with microglia serving as key initial responders. While acupuncture has demonstrated anti-inflammatory and microglia-modulating potential, its molecular mechanisms in reshaping immunological niches remain unclear. - Source: PubMed
Cao Jiang-PengLiu Xiao-XiWang Ling-FeiZhou YingZhang LinChen Xu-JuanLin Yue-XinChen Lin-LingDu Yuan-Hao - This study employs a multiomics approach to investigate the protective effects of fucoxanthin (Fu) and explore its potential association with metabolic and signaling pathways in diabetic mice induced by a high-fat diet combined with streptozotocin (STZ) administration. Diabetic model mice were randomly divided into normal control (NC), diabetic model, low-dose Fu (50 mg/kg/day), and high-dose Fu (100 mg/kg/day) groups. After 6 weeks of intervention, Fu treatment was associated with dose-dependent improvements in glucose and lipid metabolism, reduced oxidative stress, decreased expression of inflammatory cytokines (tumor necrosis factor-α [TNF-α], interleukin-6 [IL-6], and IL-1β) and renal fibrosis markers (TGF-β1, α-SMA, and Col1a1), along with notable attenuation of renal pathological damage. Exploratory analyses indicated that these phenotypic improvements were accompanied by reduced renal IDO1 expression, favorable shifts in tryptophan (Trp) metabolism, and upregulated AhR/CYP1A1 signaling. 16S rRNA sequencing revealed that Fu treatment was associated with a restoration of diabetes-altered gut microbiota β-diversity. Serum metabolomics identified that Fu administration correlated with alterations in multiple metabolites (including 5'-S-methyl-5'-thioadenosine, LPC 16:0, and bile acids), which are linked to key pathways such as Trp metabolism and bile acid biosynthesis. Network pharmacology predictions further suggested potential multitarget interactions of Fu with the PI3K-Akt and AGE-RAGE signaling pathways. Collectively, these findings indicate that Fu exerts potential renoprotective effects in diabetic mice, which are accompanied by a normalization of Trp-AhR pathway-related metabolism and concurrent attenuation of inflammatory, oxidative, and fibrotic responses. While causal functional links remain to be fully elucidated, these observations provide a preliminary basis for further mechanistic investigation and support the potential of Fu as a dietary supplement or adjunctive strategy for diabetic kidney disease (DKD). - Source: PubMed
Guo DonglinXie JiayongDong XueyunXu HaoXie YunhanLiu XinyuXu LinlinAli AsmaaChen MinZhang LeileiHe JiayuanWu LiangShao Keke - In tune with the light/dark cycle of the environment, melatonin is secreted on a circadian rhythm. After the lights go out, circulating melatonin levels gradually rise and peak in the middle of the dark phase. Herein, we studied the possible protective timing of melatonin administration on monosodium glutamate-induced cerebellar ataxia in rat models. Thirty-two adult albino male were randomly categorized into four groups: control group, MSG group (4 g/kg/day), day-time melatonin group (MSG + melatonin, 10 mg/kg/day at 9.00 a.m.), and night-time melatonin group (MSG + melatonin, 10 mg/kg/day at 9.00 p.m.). After 10 days of injections, behavioral assessments and serum melatonin were measured. Then rats were sacrificed, cerebellar immunohistopathology, oxidative stress (GPX, GR, NO, iNOS), gene expression of pro-inflammatory genes (PI3K, TNF-α, IL-6) and antioxidant genes (NRF2/HO-1) were assessed. Administration of MSG significantly caused motor deficits, increased levels of NO, INOS, PI3K, TNF-α, and IL-6 levels (p < 0.05), while significantly decreased GPX, GR, NRF2/HO-1, and serum melatonin level (p < 0.05). Histological analysis revealed that MSG exerted degenerative effects, including the presence of pyknotic Purkinje cells, with strong positive reactions for COX2. However, melatonin administration improved these parameters in both treated groups with the superiority of the night melatonin in improving motor behaviors, histological parameters, decreasing COX2 levels, INOS, PI3K, and increasing the expression of NRF2 levels, and increasing the serum melatonin levels. Night-time melatonin administration was more effective in protection against motor incoordination and cerebellar damage than day-melatonin administration. - Source: PubMed
Ahmad Alaa GamalAbd El-Fadeal Noha MArafat Horeya Erfan KorayemAhmed Dalia IbrahimAtta Rasha - Autoinflammatory syndromes are defined by episodes of recurrent fever driven by innate immune dysregulation, yet their long-term organ consequences remain largely underestimated, mostly in children. Renal AA amyloidosis represents the most perilous complication of sustained, even subclinical, inflammation, capable of progressing silently to irreversible renal failure. In pediatric cohorts, the interval between autoinflammatory disease onset and amyloidosis diagnosis spans nearly a decade, an actionable window that current surveillance frameworks have not adequately addressed. This review examines the pathophysiological linking chronic cytokine overproduction to renal amyloid deposition in children with autoinflammatory syndromes, evaluates emerging subclinical biomarkers of early renal injury, identifies relevant diagnostic pitfalls, and proposes a structured renal surveillance framework for at-risk pediatric populations. This comprehensive review has been conducted analyzing studies reporting renal outcomes, biomarker data, or therapeutic interventions in pediatric patients with monogenic or polygenic autoinflammatory conditions. No date restriction was applied, with emphasis placed on publications from 2015 onward reflecting contemporary treatments and diagnostic standards. An overproduction of interleukin (IL)-1β and IL-6 drives serum amyloid-A accumulation that may persist measurably during intercritical periods, preceding overt proteinuria by years in most young patients with autoinflammatory syndromes. Urinary neutrophil gelatinase-associated lipocalin (NGAL) is significantly elevated in attack-free children with familial Mediterranean fever (FMF) compared to healthy controls, representing an early and sensitive marker of tubular stress. Shear wave elastography has demonstrated measurable increases in renal tissue stiffness in pediatric FMF patients, correlating with subclinical inflammatory activity. Critically, nutcracker syndrome has emerged as the leading cause of proteinuria in colchicine-treated FMF cohorts, accounting for up to 67.5% of proteinuria cases and representing a clinically significant confounder. IL-1 inhibition with either anakinra or canakinumab has demonstrated histological regression of established amyloid deposits in different cohorts of pediatric patients, reinforcing the potential therapeutic value of earlier identification and intervention before overt irreversible glomerular damage comes out. Renal amyloidosis in autoinflammatory syndromes is a plausibly preventable outcome when subclinical injury is identified and treated within the pre-amyloid window in the pediatric age. Conventional reliance on 'proteinuria' as the primary surveillance threshold is potentially misleading. A biomarker-guided monitoring approach incorporating serum amyloid-A, urinary NGAL, and renal elastography might offer a clinically actionable pathway toward earlier nephrology referral and targeted IL-1 blockade, with the potential to improve renal prognosis of these children. - Source: PubMed
Publication date: 2026/09/01
Arsiwala NaqiyaRigante Donato