Marmoset IL-6 ELISA kit (supernatant only)
- Known as:
- Marmoset Interleukin-6 Enzyme-linked immunosorbent assay test reagent (supernatant only)
- Catalog number:
- CT346A
- Product Quantity:
- 5-plate*
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- Marmoset IL-6 ELISA kit (supernatant only)
Related genes to: Marmoset IL-6 ELISA kit (supernatant only)
- 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
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- Ischemic stroke (IS) triggers neuroinflammation that drives neuronal dysfunction and tissue injury. Resident central nervous system macrophages critically contribute to IS-induced injury through inflammatory infiltration and cytokine secretion. Methylophiopogonone A (MOA), a flavonoid from Ophiopogon japonicus, protects against heart and liver injury, but its role in IS-induced brain injury remains unclear. Here, we investigated whether MOA attenuates neuroinflammation and brain injury in a mouse IS model and explored its molecular mechanism in macrophage inflammatory activation. MOA treatment reduced brain infarct volume and neurological deficits in transient middle cerebral artery occlusion (tMCAO) mice. It also significantly decreased the secretion of pro-inflammatory cytokine (IL-2, IL-6, IL-1β, IL-18, TNF-α) and TGF-β, and suppressed M1 activation marker expression (IL-6, TNF-α, iNOS) in brain tissue. Immunofluorescence revealed that MOA reduced neutrophil and monocyte-derived macrophage infiltration into ischemic lesions, inhibited macrophage iNOS expression, and suppressed NF-κB p65 phosphorylation. Mechanistically, MOA directly bound the NF-κB p65 subunit, inhibiting its phosphorylation and nuclear translocation in macrophages. This suppressed M1 activation gene expression (IL-6, TNF-α, iNOS) and reduced pro-inflammatory cytokine secretion (IL-6, IL-1β, IL-18, TNF-α). Collectively, these findings demonstrate that MOA protects against tMCAO-induced ischemic injury by inhibiting NF-κB signaling-mediated M1 activation of macrophages and reducing the infiltration of both macrophages and neutrophils. These results position MOA as a potential therapeutic agent for neuroinflammation and brain injury associated with IS. - Source: PubMed
Publication date: 2026/07/30
Yao JieZhu Fang-FangWei Xue-ZhiZheng Yun-QiuGui Zhong-HaoYang ZhengSun Zhong-Wu - Anthocyanins (ACNs) are a sub-group of dietary polyphenols with well-studied safety, potency and efficacy against chronic inflammation and age-related diseases. However, the unified molecular mechanism remains not fully defined. This review integrates recent evidence on dietary ACNs, with emphasis on food sources, processing stability, and bioavailability, to elucidate how ACNs orchestrate health benefits via the MAPK signaling pathway. This review highlights an important, dualistic regulation: while suppressing stress-responsive p-p38 and p-JNK to prevent NF-κB-driven cytokine production and senescence-associated secretory phenotypes, ACNs facilitate the promotion of p-ERK1/2 to enhance the CREB-BDNF axis and promote synaptic plasticity. Translational validations involving various models and clinical trials demonstrate that ACNs can efficiently alleviate systemic inflammation (CRP, IL-6) and significantly prevent p-JNK. These effects are highly dependent on dietary intake, food matrix composition, and processing conditions that influence the formation of bioactive metabolites. In this context, dietary ACNs represent promising candidates for functional food development owing to their precise bidirectional modulation of the MAPK pathways. Future studies should prioritize mechanism-driven randomized controlled trials using physiologically relevant concentrations of microbiota-derived metabolites. - Source: PubMed
Publication date: 2026/07/06
Luo JincanLuo JinhaiHan BinchengXu Baojun - Alcohol-induced gastric injury caused by excessive alcohol consumption is characterized by oxidative stress and inflammatory cascades that form a vicious cycle, leading to progressive gastric mucosal damage. Existing interventions, which are limited in their functional scope, are unable to effectively address this complex condition, underscoring the urgent need to develop safe and effective protective strategies. Here, a novel disulfide-crosslinked hydrogel was constructed using poly(γ-glutamic acid) (γ-PGA) and lipoic acid (LA), with arginine (Arg) incorporated via hydrogen bonding to obtain Arg-gel, as characterized by NMR and FT-IR. The 8% (w/v) gel exhibits excellent mucosal adhesion and extends the retention time in the stomach from 15 to 30 min to 2-4 h. In vitro, Arg-gel demonstrated dose-dependent antioxidant activity and significantly reduced intracellular ROS in alcohol-stimulated GES-1 cells, while also suppressing pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and restoring mitochondrial function. In a mouse model of acute alcohol-induced gastric injury, Arg-gel markedly reduced the ulcer index and facilitated the restoration of mucosal architecture and PGE2 levels. No significant toxicity was observed in a 14-day biosafety assessment. Collectively, Arg-gel exhibits promising gastroprotective effects and biosafety, offering a novel strategy for gastric mucosal protection. - Source: PubMed
Publication date: 2026/06/24
Wang Xin-ChuangLuo Feng-XianXu YuChen Li-HangWu DiDu Yi-NanHu Jiang-Ning - In this study, the natural active ingredient glycyrrhizic acid (GA) was used to replace traditional synthetic surfactants to construct GA-functionalized Tanshinone IIA (TSA) nanostructured lipid carriers (TSA@GA NLCs). The prepared TSA@GA NLCs had a particle size of 268.7 ± 2.3 nm and an encapsulation efficiency of 84.90 ± 5.45%. They exhibited a spherical core-shell structure, demonstrated good preliminary short-term stability, and displayed in vitro release profiles consistent with those of an oral sustained-release delivery system. In a carbon tetrachloride (CCl)-induced mouse model of liver fibrosis, TSA@GA NLCs significantly reduced serum transaminase levels (ALT decreased from 246.90 ± 9.73 U/L in the model group to 83.82 ± 2.87 U/L, AST from 348.77 ± 7.66 U/L to 139.87 ± 4.31 U/L), and reversed levels of inflammatory factors (TNF-α from 62.57 ± 1.33 μg/L to 18.83 ± 0.73 pg/mL; IL-1β and IL-6 showed consistent trends) and oxidative stress markers (MDA decreased from 1.88 ± 0.11 nmol/mg prot to 1.25 ± 0.03 nmol/mg prot, GSH increased from 11.36 ± 0.49 nmol/mg prot to 14.70 ± 1.00 nmol/mg prot), improved histopathological damage to liver tissue, reduced collagen deposition, and suppressed α-SMA expression. The TSA@GA NLCs group demonstrated significantly better improvement across all indicators. Furthermore, this study preliminarily investigated changes in protein expression in the NRF2/NF-κB pathway; however, molecular interactions between these pathways require further validation. The findings indicate that GA possesses dual functions of structural stabilization and combination-enhanced therapy. Through an integrated "delivery-therapy" strategy, TSA@GA NLCs effectively enhanced the antifibrotic efficacy of TSA, providing new insights for the design of delivery systems for active ingredients in traditional Chinese medicine. - Source: PubMed
Publication date: 2026/08/22
Wu JijiaoWen LinSun ZihaoLiu XiaolianChen LipingLi Xiaofang - 6PPD and its ozonation product 6PPD-quinone (6PPD-Q) are widespread tire-derived pollutants. This study combined network toxicology, clinical transcriptomics, molecular docking, and experimental validation to investigate their intestinal toxicity mechanisms and potential molecular relevance to inflammatory bowel disease (IBD), including Crohn's disease (CD) and ulcerative colitis (UC). Database screening identified 213 predicted targets for 6PPD and 165 for 6PPD-Q. Venn analysis identified 160 and 61 targets shared between 6PPD and CD- and UC-associated genes, respectively, whereas 112 and 105 targets were shared between 6PPD-Q and CD- and UC-associated genes, respectively. Network analyses showed that 6PPD-associated targets were mainly enriched in inflammatory signaling and oxidative stress-related pathways involving candidate hubs such as HIF1A, IL1B, IL6, and PTGS2. In comparison, 6PPD-Q-associated targets were enriched in kinase-signaling and mucosal-repair-related pathways involving HCK, KDR, LYN, EGFR, and MAPK14. Molecular docking predicted favorable binding poses between the compounds and the selected candidate targets, with docking scores ranging from -6.0 to -8.8 kcal/mol. Comparisons with clinical transcriptomic datasets further showed that several candidate targets were dysregulated in inflamed IBD tissues. In vivo, repeated exposure of C57BL/6 mice to 6PPD or 6PPD-Q for 40 days resulted in colon injury, reduced expression of intestinal tight-junction proteins, and increased expression of inflammatory mediators. In RAW264.7 macrophages, both compounds induced dose-dependent cytotoxicity, ROS production, and increased proinflammatory gene expression. These findings demonstrate that 6PPD and 6PPD-Q induce intestinal injury, oxidative stress, and inflammatory activation in experimental models and affect molecular targets and pathways implicated in IBD. Further studies using established experimental IBD models are warranted to determine whether these compounds exacerbate pre-existing intestinal inflammation or influence disease severity. - Source: PubMed
Publication date: 2026/08/22
Zhang YixuanLuo YuyangWang SiyiLi Ze