Mouse IL-6 ELISPOT kit
- Known as:
- Mouse Interleukin-6 ELISPOT reagent
- Catalog number:
- CT436-PB5
- Product Quantity:
- 5-plate
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- Mouse IL-6 ELISPOT kit
Related genes to: Mouse IL-6 ELISPOT 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: Mouse IL-6 ELISPOT kit
Related articles to: Mouse IL-6 ELISPOT kit
- Determining the pathogenesis of endometriosis remains a major challenge in contemporary gynecology, and the investigation of alterations in cellular immunity may provide important insights into this issue. A comprehensive search of electronic databases (PubMed, The Cochrane Library, ClinicalTrials.gov, Scopus, Embase, and Google Scholar) identified 24 studies meeting the inclusion criteria for qualitative synthesis. The primary analysis compared the concentration of IL-4 in peripheral blood (MD = 1.32, 95% CI: -15.00 to 17.63, p = 0.87); the secondary compared the concentration of HLA-DR-macrophages (MD = -2.62, 95% CI: -8.98 to 3.73, p = 0.42) and HLA-ABC-macrophages (MD = -6.84, 95% CI: -23.94 to 10.26, p = 0.43) in peritoneal fluid; the third compared the IL-6 concentration in peritoneal fluid (MD = 338.00, 95% CI: 85.02 to 590.98, p = 0.009); the fourth compared the NK-cell level in peritoneal fluid (MD = 6.75, 95% CI: -12.42 to 25.91, p = 0.49); the fifth compared the level of NK-cells in ectopic and eutopic endometrium (MD = -9.12, 95% CI: -24.39 to 6.15, p = 0.24) between endometriosis and control groups. Overall, the included studies suggest that signaling pathways involving T lymphocytes, monocytes, macrophages, and natural killer cells are altered in patients with endometriosis. - Source: PubMed
Adamyan LeilaPivazyan LauraKurbatova KristinaBarsegyan SonaMailova KarinaStepanian Assia - Traumatic Brain Injury (TBI) is a major cause of mortality and disability worldwide and is associated with oxidative stress, neuroinflammation, and neurotransmitter imbalance. Arbutin, a naturally occurring glycoside with known antioxidant and anti-inflammatory properties, has the potential to modulate neurochemical alterations following brain injury. The present study was designed to evaluate the neuroprotective effects of arbutin in a zebrafish model of TBI induced by a novel non-invasive mechanical impact method termed "force-induced TBI." Adult zebrafish were randomly divided into seven groups (n = 14 per group): normal control, TBI control, arbutin per se, arbutin-treated groups (25, 50, and 100 mg/kg, i.p.), and a co-treatment group receiving arbutin (100 mg/kg) co-administrated with chrysin (25 mg/kg), a known modulator of the Nrf2/NF-κB signaling pathway. Behavioural assessments, including the open field test, novel tank diving test (NTDT), T-maze, and novel object recognition test (NORT), were conducted on days 1, 4, and 7 to evaluate locomotion activity, anxiety-like behaviour, spatial memory, and recognition ability, respectively. Following behavioural evaluation, brain tissues were analysed for oxidative stress markers (MDA, nitrite, GSH, and SOD), neurotransmitter levels (GABA and glutamate), pro-inflammatory cytokines (TNF-α, IL-1β, and IL-6), and histopathological alterations. Immunohistochemical analysis of Nrf2 and NF-κB was also performed. The results demonstrated that arbutin significantly improved behavioural performance, restored oxidative balance, normalized neurotransmitter levels, and attenuated neuroinflammatory responses. Furthermore, arbutin treatment was associated with increased Nrf2 immunoreactivity and reduced NF-κB immunoreactivity in a dose-dependent manner. The co-treatment with chrysin also exhibited protective effects, supporting its potential modulatory role in oxidative stress and these effects are associated with modulation of oxidative stress, neuroinflammation, neurotransmitter imbalance, and Nrf2/NF-κB immunoreactivity. These findings suggest that arbutin possesses neuroprotective potential against secondary brain injury and is associated with modulation of oxidative stress, inflammatory responses, and Nrf2/NF-κB immunoreactivity. - Source: PubMed
Publication date: 2026/07/29
Singh Shamsher - Rutin, a bioactive flavonoid widely present in medicinal plants such as Fagopyrum esculentum, Ruta graveolens, and citrus species, has been traditionally used for inflammatory conditions, including joint disorders. Despite its long-standing ethnomedicinal use, a comprehensive mechanistic understanding of its role across different types of arthritis remains limited. This review aims to systematically evaluate the pharmacological effects and molecular mechanisms of rutin in rheumatoid arthritis, gouty arthritis, osteoarthritis, and Psoriasis, integrating ethnopharmacological relevance with modern experimental evidence. A comprehensive literature search was conducted across databases including PubMed, Scopus, and Web of Science. Preclinical in vivo, in vitro, and mechanistic studies investigating rutin in arthritic models were included. Data were synthesized to identify key molecular targets, signaling pathways, and therapeutic outcomes. Rutin demonstrated significant anti-arthritic effects across multiple models. In rheumatoid arthritis, rutin reduced inflammatory cytokines (TNF-α, IL-6), oxidative stress, and joint damage via inhibition of NF-κB and iNOS signaling. In gout, rutin lowered uric acid levels by inhibiting xanthine oxidase and suppressing NLRP3 inflammasome activation. In osteoarthritis, rutin protected cartilage integrity by modulating extracellular matrix degradation and regulating NF-κB/MAPK, SIRT1, and RhoA/ROCK pathways. In Psoriasis, rutin attenuated keratinocyte proliferation and inflammation through JAK/STAT inhibition and activation of the Nrf2 antioxidant pathway. Additionally, advanced delivery systems such as nanoparticles and hydrogels enhanced its bioavailability and therapeutic efficacy. Rutin exhibits multi-target anti-arthritic potential supported by both traditional use and modern pharmacological evidence. Its ability to modulate key inflammatory and oxidative pathways highlights its potential as a phytopharmaceutical candidate for arthritis management. Further clinical validation and standardization are required to translate these findings into therapeutic applications. - Source: PubMed
Publication date: 2026/07/29
Nazir Muhammad MuzammilAshraf Asma - Intervertebral disc degeneration (IVDD) is a degenerative disease characterized by degradation of the extracellular matrix (ECM) in the nucleus pulposus, disruption of the fibrous ring structure, and imbalance of the inflammatory microenvironment. It is the main cause of chronic low back pain. Its pathogenesis is closely related to cellular aging and immune inflammation. Aging nucleus pulposus cells release pro-inflammatory factors such as IL-6 and TNF-α through the secretion of senescence associated secretory phenotype (SASP), recruiting M1 macrophages to infiltrate and forming a vicious cycle of "aging inflammation matrix destruction." This study systematically analyzed the molecular mechanism by which kaempferol improves IVDD through multi-target regulation by integrating bioinformatics analysis, animal experiments, and cell models. Bioinformatics screening revealed significant abnormal expression of genes such as AURKB, CCNB1, AXL, NEK6, and PTK2 in IVDD degenerated tissues. Downregulation of CCNB1 induced G2/M phase arrest by inhibiting CDK1 activity, while activation of GSK3B inhibited the Wnt signaling pathway by phosphorylating β-catenin, exacerbating ECM catabolism. Proteomics further confirms that the NOX4 mediated ROS-p38 MAPK pathway promotes cell apoptosis and SASP secretion. Immune infiltration analysis showed that M1 macrophages were significantly enriched in degenerated intervertebral discs, and their secreted IL-6 and TNF-α amplified the inflammatory cascade by activating the NF-κ B pathway. Animal experiments have shown that intervention with kaempferol can partially restore the intervertebral disc height index (DHI), downregulate the levels of IL‑1β and TNF‑α, upregulate the expression of CCNB1 and AURKB (which were downregulated in the IVDD model), thereby alleviating G2/M phase arrest and promoting cell cycle progression, inhibit AXL and PTK2, and reduce macrophage infiltration. Mechanistically, kaempferol inhibits NOX4 activity by clearing ROS, blocking the vicious cycle of oxidative stress‑inflammation; by regulating the NEK6/NF‑κB axis, the expression of MMP‑3 and ADAMTS‑4 is reduced, delaying ECM degradation; and improve the immune microenvironment by promoting macrophage polarization towards the M2 phenotype. In addition, kaempferol can reverse the metabolic imbalance mediated by GSK3B. This study reveals for the first time that kaempferol upregulates core gene networks such as AURKB and CCNB1 while suppressing AXL through the "anti‑inflammatory anti‑aging" dual pathway, thereby breaking the "aging‑immunity" crosstalk and restoring cell cycle homeostasis, providing a new strategy for natural compound intervention in IVDD treatment. - Source: PubMed
Publication date: 2026/07/29
Li DongyangWu XiaofeiChen FengSong ChaoXu Zhiwei - Understanding the earliest pathological changes in Alzheimer disease (AD) is critical for improving early intervention strategies. However, the relationship between amyloid plaque characteristics and early behavioral and molecular alterations remains unclear. We used 6-month-old female APPswe/PS1dE9 mice, a model of early amyloid-dominant pathology, to assess cognition and emotionality across a battery of behavioral tests. Amyloid plaques were quantified using Congo red staining; RT-qPCR and GFAP immunoreactivity were used to assess molecular and glial changes. APPswe/PS1dE9 mice exhibited increased anxiety-like behavior without significant changes in overall locomotor activity. Small plaques (<100 μm2) predominated across all regions; however, behavioral measures of hyperactivity and anxiety correlated specifically with the density and size of large (>200 μm2) plaques. Gene expression changes, including altered SYP, IGF1, TNF, and IL6 expression, were observed primarily in the midbrain and did not correlate with amyloid plaque characteristics. These findings demonstrate that large amyloid plaques, rather than total plaque burden, are selectively associated with early behavioral alterations in APPswe/PS1dE9 mice. Moreover, the midbrain emerges as an early site of molecular dysregulation despite limited plaque deposition. Together, these results support the use of 6-month-old APPswe/PS1dE9 mice as a model of early, amyloid-dominant stages of AD. - Source: PubMed
Publication date: 2026/07/29
Sitdikova KseniiaTsoy AndreyChaprov Kirill Dde Munter JohannesSvirin EvgeniyTorosyan HamletYenkoyan KonstantinAskarova SholpanSteinbusch Harry WAnthony Daniel CStrekalova Tatyana