Cymax Mouse IL-6 ELISA Kit
- Known as:
- Cymax Mouse Interleukin-6 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- lf-ek0270
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Abfrontier
- Gene target:
- Cymax Mouse IL-6 ELISA Kit
Related genes to: Cymax Mouse 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: Cymax Mouse IL-6 ELISA Kit
Related articles to: Cymax Mouse IL-6 ELISA Kit
- Icariside II (ICS II), a PDE5 inhibitor, is a flavonoid glycoside and primary metabolite of icariin, derived from the herb Herba epimedii, and exhibits promising neuroprotective potential in various pre-clinical studies. The current review provides evidence that ICS II shows neuroprotective potential against various neurological disorders, mainly including Alzheimer's disease, Parkinson's disease and Cerebral ischemia through modulating neuroinflammation, oxidative stress, neural apoptosis, neurogenesis, mitochondrial and cognitive dysfunction. It regulates multiple signalling pathways including PI3K/Akt, Keap1/Nrf2, TLR4/MyD88/NF-κB, cGMP/PKG/CREB, TGFB1/Smad, Wnt/β-catenin signaling and BDNF/TrkB/CREB. The pre-clinical evidence suggests that ICS II attenuates oxidative stress through increasing antioxidant enzymes SOD, GSH, catalase, and HO-1, with decreasing MDA and lipid peroxidation. Neuroinflammation is suppressed by inhibition of pro-inflammatory cytokines and down-regulation of IL-1β, IL-6, TNF-α, COX-2, iNOS levels and up-regulation of tight-junction proteins like occludin, claudin-5, ZO-1. Apoptosis is regulated via altering PARP, Bcl-2, Bax/Bcl-2 ratio and reducing caspase-3 activation. Mitochondrial dysfunction is ameliorated by restoring Complex I activity and increasing mitofusin-1/2 expression and reducing mitochondrial fission factors. Collectively, these molecular mechanisms show promise for ICS II as a potential candidate in different in vivo and in vitro studies of neurological disorders. - Source: PubMed
Solanki AshutoshSharma KhushiJain JagratiSingh Niraj KumarKrishnamurthy Praveen T - This study aims to explore the protective effect of electroacupuncture (EA) on myocardial ischemia-reperfusion injury (MIRI) and decipher the molecular mechanism. Forty male SD rats were randomly allocated into four groups: sham, model (ischemia/reperfusion, I/R, MI group), I/R combined with ST36 (ST36 group), and I/R combined with sham acupuncture (MI+sham group). The MIRI model was established by ligation and reperfusion of the left anterior descending coronary artery. EA stimulation was applied at Neiguan (PC6) and Zusanli (ST36) in the ST36 group. Echocardiography, Evans blue-TTC double staining, ELISA and multi-omics techniques were adopted to evaluate therapeutic efficacy and analyze molecular characteristics. The results demonstrated that EA markedly reduced myocardial infarct size, improved cardiac systolic function, and decreased serum levels of IL-6, IL-1, and TNF-α as well as the expression of high mobility group box 1 (HMGB1) in the myocardial tissue. A total of 6 676 proteins were identified differential proteomics analysis. One hundred and eighty-seven differentially expressed proteins were identified between the MI group and the sham group, among which the expression of 141 proteins was reversed after EA intervention. These proteins were mainly enriched in signaling pathways related to mitochondrial autophagy and apoptosis. Metabolomics analysis screened out 454 differential metabolites, which were predominantly involved in sphingolipid metabolism and alanine-aspartate-glutamate metabolism pathways. This study indicates that EA alleviates myocardial damage in the rat model of MIRI by suppressing inflammatory responses and regulating signaling pathways associated with myocardial structural maintenance, energy metabolism, and cell survival. The therapeutic mechanism of EA involves the synergistic modulation of multiple targets and pathways, providing experimental evidence for the comprehensive treatment of MIRI. - Source: PubMed
Wang HuanLi YuanCao RuihuaHu YazhuoZhang XinxinDou ZhongmeiLi DanWang YiranWang HeranJia Jianjun - Neuroinflammation driven by activated microglia is an important component of secondary injury after traumatic brain injury (TBI), but the underlying molecular mechanisms remain incompletely understood. Here, we investigated the role of microglial Toll-like receptor 7 (TLR7) in TBI-induced neuroinflammation and evaluated the therapeutic effect of the TLR7-targeting compound Enpatoran (M5049). Analysis of public single-cell transcriptomic datasets showed that TLR7 is preferentially expressed in microglia among resident brain cells. In the controlled cortical impact (CCI) mouse TBI model, TBI increased TLR7 expression in microglia and elevated the abundance of cleaved-TLR7 in the peri-contusional cortex. Knockdown of the asparaginyl endopeptidase (AEP) attenuated TLR7 cleavage and downstream signaling in cultured microglia. Deletion of AEP decreased cleaved-TLR7 and inflammatory marker expression in TBI mice, indicating an AEP-mediated proteolytic processing of TLR7 and suggesting TLR7's involvement in TBI inflammation. Global TLR7 deletion in mice failed to reduce TBI-induced inflammation and was accompanied by marked TLR8 upregulation. In contrast, inducible microglia-specific TLR7 deletion in mice attenuated CD86, TNF-α, and IL-1β expression without a pronounced TLR8 upregulation. The TLR7 inhibitor M5049 suppressed TLR7 agonist-induced inflammation in cultured microglia without inhibiting mouse TLR8. In TBI mice, treatment with M5049 at 0.1, 0.3, and 3 mg/kg all significantly reduced TBI-induced IL-1β and IL-6 mRNA expression. Pharmacological tests further showed that M5049 is effective in suppressing TBI-induced microglial activation and inflammatory cytokine secretion in wild-type mice but lost this efficacy in TLR7 knockout mice. Therefore, M5049's anti-inflammatory action relies on the presence of TLR7. Additionally, M5049 was not able to rescue glutamate- and HO-induced cell death in HT22 mouse hippocampus neuronal cells, or broadly suppress the examined peripheral immune transcriptional program. These findings identify microglial TLR7 as an important player in TBI-induced neuroinflammation and support a predominantly TLR7-dependent anti-inflammatory effect of M5049. - Source: PubMed
Publication date: 2026/08/24
Du Yi-TengMa Xiao-LiGao Shu-HuiWang Yan-XiaLiu YanFeng Xue-MeiFan ChenChen Hong-ZhuanSong Ming-Ke - Patients with chronic rhinosinusitis with nasal polyps (CRSwNP) exhibit heterogeneous responses to oral glucocorticoids (GCs), but the biological basis of this variability remains unclear. - Source: PubMed
Publication date: 2026/08/24
Zhang Ying-YingDing Xin-YuLu Mei-PingChen Yan-BingYuan YeJiang LinZhang MinCheng Lei - Plasmid-borne mcr-1 has been disseminated globally through the food chain, raising major concerns in food safety. We previously reported that mcr-1 plasmids carrying the transcriptional regulator gene ecaR activate surface polysaccharide production in Escherichia coli, converting a rough phenotype to smooth and enhancing virulence in a murine model. Here, we examined host-side consequences of this surface polysaccharide remodeling using E. coli isolates originating from human stool and retail raw chicken. In RAW 264.7 macrophages, strains harboring both mcr-1 and ecaR elicited markedly higher TNF-α and IL-6 production than the wild-type strain, and surface polysaccharide-enriched extracts from these strains induced cytokines dose-dependently. In a Galleria mellonella model, live-bacterial infection with strains carrying both genes produced accelerated lethality, and injection of equal doses of surface polysaccharide-enriched extracts, without live bacteria, significantly increased larval mortality, suggesting that the remodeled surface polysaccharide-enriched preparations may contribute to virulence-associated lethality. Strains co-harboring mcr-1 and ecaR also survived better in normal human serum, indicating enhanced resistance to complement-mediated killing. Similar macrophage cytokine responses were observed in multiple retail chicken-derived E. coli isolates. A complementary BLASTn survey of 361 ecaR-positive E. coli records showed that ecaR is predominantly carried on IncI2 plasmids, in which mcr co-carriage is concentrated, but is also distributed across IncFIB and pEC4115-like plasmids. Importantly, mcr-1 and ecaR co-occurrence was enriched among poultry-associated records. These findings highlight a food-safety-relevant consequence of mcr-1 dissemination beyond antibiotic resistance. - Source: PubMed
Publication date: 2026/07/18
Ahn EunbyeolKim JinshilShin HojunRyu SangryeolJeon Byeonghwa