Chicken Interleukin 6,IL-6 ELISA Kit
- Known as:
- Chicken Interleukin 6,Interleukin-6 Enzyme-linked immunosorbent assay test Kit
- Catalog number:
- E0003Ch
- Product Quantity:
- 48T
- Category:
- Elisa Kits
- Supplier:
- JING
- Gene target:
- Chicken Interleukin 6 IL-6 ELISA Kit
Related genes to: Chicken 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: Chicken Interleukin 6,IL-6 ELISA Kit
Related articles to: Chicken Interleukin 6,IL-6 ELISA Kit
- In this work, Eucalyptus salubris seeds extract (ESS) was characterized using liquid chromatography (LC) coupled to mass spectrometry (MS), and its in vitro and in vivo anti-inflammatory properties were evaluated. Through LC-MS and MS analysis, flavanonols and monounsaturated fatty acids were found to be the most abundant components, while unreported galloylated flavanonols were profiled. ESS attenuated the denaturation of Bovine Serum Albumin (BSA), significantly stabilized rats Red Blood Cells (RBC) membranes, and inhibited both Cyclooxygenase-1 (COX-1) and Cyclooxygenase-2 (COX-2) enzymes, indicating its ability to reduce inflammation. The in vivo study showed that ESS significantly reduced the carrageenan-induced paw edema in rats and normalized the inflammatory cytokines Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-6 (IL-6) levels. In addition, ESS alleviated formaldehyde-induced arthritis symptoms through a remarkable reduction in oxidative stress biomarkers (evidenced by decreased Malondialdehyde (MDA), Glutathione (GSH), and Nitric Oxide (NO) levels, along with increased Superoxide Dismutase (SOD) and Catalase (CAT) activities), as well as the restoration of the hematological profile (reduction in white blood cell (WBC) count and erythrocyte sedimentation rate (ESR), accompanied by an increase in red blood cell (RBC) count and hemoglobin (Hb) levels). These effects are largely attributable to the richness of ESS in phenolic compounds, flavonoids, and other bioactive secondary metabolites. Collectively, these findings supported the therapeutic potential of E. salubris extract as a natural source of anti-inflammatory and antioxidant agents, warranting further investigation for potential pharmaceutical or nutraceutical applications. - Source: PubMed
Publication date: 2026/04/22
Ferjani NouhaMekky Reham HassanContreras María Del MarJalouli MarouaFeriani AnouarTir MeriamSaadaoui EzzeddineHarrath Abdel HalimTlili Nizar - Hypoxia is known to disrupt embryonic organogenesis and increase the risk of neonatal respiratory disorders. The Hippo pathway is crucial in regulating organ development, size, and cell proliferation. However, the mechanism of how hypoxia affects lung development through this pathway remains unclear. - Source: PubMed
Publication date: 2026/04/22
Liao Zih-AnTsao Po-NienChen Chung-MingChung Kian FanLee Po-HengChuang Kai-JenChuang Hsiao-Chi - This study examined serum brain injury markers and their associations with disease features, cytokines associated with microglial activation in lupus and cognitive dysfunction (CD) in adolescents with childhood-onset SLE (cSLE). - Source: PubMed
Publication date: 2026/04/22
Mwizerwa OscarLedochowski JustineRamanathan GaneshTal Tala EMossad Sarah IZapparoli BusiNg LawrenceJeyanathan AshaDavis AdrienneHiraki Linda TLevy Deborah MWither JoanTouma ZahiDanguecan AshleyYeh AnneKnight Andrea M - Liver fibrosis represents an abnormal wound-healing response to chronic hepatic injury. It is characterized by the excessive production and deposition of extracellular matrix components, ultimately resulting in the formation of a fibrotic scar. Visnagin, a phytochemical, has antioxidants and anti-inflammatory activity and modulates apoptosis; however, the role of visnagin in liver fibrosis has not been previously explored. Herein, we have induced liver fibrosis using thioacetamide (TAA; 200 mg/kg) through the intraperitoneal (i.p.) route every third day for 8 weeks in Sprague Dawley rats. Visnagin (5 and 10 mg/kg) co-treatment was given via the i.p. route every day for 8 weeks. At the end of the visnagin intervention, various biochemical, oxidative stress parameters, histopathological assessments, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analyses were performed. Visnagin administration resulted in a significant decrease in the liver-to-body weight ratio and liver injury markers, including alanine transaminase, aspartate aminotransferase, and alkaline phosphatase. Additionally, visnagin attenuated TAA-induced oxidative stress by restoring levels of malondialdehyde, nitrite, and superoxide dismutase. Histopathological assessments confirmed the hepatoprotective effects of visnagin against TAA-induced liver injury, as evidenced by a reduction in hepatocyte damage and collagen deposition. Further, at a molecular level, visnagin treatment reduces the expression of caspase-3 and genes related to inflammation (TLR4, TNF-α, IL-6, NLRP3) and fibrosis (α-SMA, Col1A1, TGF-β, MMP9, and TIMP1) in TAA-treated rats. - Source: PubMed
Publication date: 2026/04/22
Goswami YogenderYadav PoonamSingh Sumeet KumarNavghare Akshay AmrutaRajput SonuKhurana AmitBhatti Jasvinder SinghNavik Umashanker - Escherichia coli (E. coli) is a leading cause of invasive bacterial infections in humans. Pathogenic E. coli is not only the major etiological agent of enteric/diarrheal disease and urinary tract infections, but also among the most common causes of sepsis and meningitis. Caspase-8 is known to regulate apoptotic and pyroptotic cell death in response to bacterial and viral infections. Here we demonstrate that caspase-8 plays a critical role in E. coli-induced macrophage apoptosis in vitro and in regulating immune response and host death in vivo. Incubation of mouse bone marrow derived macrophages (BMDMs) with an E. coli K1 strain CE10 triggered robust cell death, which is independent of the NAIP/NLRC4/caspase-1/GSDMD pathway. CE10 stimulation induced caspase-8 activation, and macrophages deficient in caspase-8 and RIPK3, but not RIPK3 alone, were protected from CE10-induced cell death. In an intraperitoneal injection sepsis model, E. coli-induced IL-1β, TNF-α, and IL-6 production was markedly reduced in caspase-8-/-/RIPK3-/- mice, compared with RIPK3-/- or wild type mice. Accordingly, the survival rate was significantly improved in caspase-8-/-/RIPK3-/- mice. Moreover, caspase-8 deficiency attenuated CE10-induced NF-κB activation and cytokine production in BMDMs. Together, our findings identify caspase-8 as a central mediator of E. coli-induced cell death, immune response, and establish its critical contribution to host mortality during E. coli infection. - Source: PubMed
Chai ZhuodongZhou YuqiYang LingZhang YanHossain SukriaZhang GuoyingQi JiaqianZhang ZiranShiroishi ToshihikoWei YinanLi Zhenyu