IL-6, Human(CHO-expressed) Protein
- Known as:
- Interleukin-6, Human(CHO-expressed) Protein
- Catalog number:
- z03134-50
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- IL-6 Human(CHO-expressed) Protein
Related genes to: IL-6, Human(CHO-expressed) Protein
- 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: IL-6, Human(CHO-expressed) Protein
Related articles to: IL-6, Human(CHO-expressed) Protein
- Obese, osteoporotic patients with intertrochanteric fractures face higher surgical risks and delayed recovery. The "Gold Wrist," an auxiliary curved guiding instrument for proximal femoral nail anti-rotation (PFNA), was developed to assist guidewire placement and improve procedural efficiency. - Source: PubMed
Publication date: 2026/07/02
Wu ZhonghanLi JianyangMao ShitanLu JingtaoZhao YaoYu ShuishengTian DashengJing JuehuaAo RongguangXu Xinzhong - Human breast milk is a complex bioactive fluid containing multi-functional components that support many infant physiological functions. Maternal diet has been demonstrated to influence human milk components; however, how maternal diet impacts inflammatory markers in human milk remains unclear. This study investigated the association between maternal dietary inflammatory status, assessed using the Dietary Inflammatory Index (DII), and the profile of inflammatory markers in breast milk from healthy lactating women, quantified using cytometric bead array. Dietary intake of lactating mothers (n = 101) was assessed using a 24-hr food recall and categorised using the DII as either pro-inflammatory (score > 0) or anti-inflammatory (score < 0). Thirteen inflammatory markers were quantified in breast milk by flow cytometric bead array (13-plex panel: IL-4, IL-2, IP-10, IL-1β, TNF-α, MCP-1, IL-17A, IL-6, IL-10, IFN-γ, IL-12p70, IL-8, free active TGF-β1). All participant diets were categorised as anti-inflammatory diets (DII score range -4.83 to -1.22). Participants' food intake aligned with dietary guidelines (AUSNUT 2023) for lactating women, with most analysed food parameters classified as anti-inflammatory (19/27). Inflammatory marker analysis revealed a chemokine-dominant profile in breast milk with IP-10, MCP-1 and IL-8 present at the highest concentrations and detected in > 96% of participant human milk samples MCP-1 concentration was weakly associated with DII score (p = 0.025, r2 -0.23, Spearman correlation). This study is the first to investigate the inflammatory index of maternal diets in lactating mothers and characterise inflammatory markers in human milk. Further research is required to fully elucidate the relationship between dietary inflammatory status and inflammatory markers in breast milk and their potential impact on infant health, especially of a more diverse cohort. - Source: PubMed
Publication date: 2026/07/02
Slegers Courtney BHolmes Mark ABiddulph CarenMaher JudithSmoll Nicolas RoydonDean Melinda M - Inflammatory bowel disease (IBD) is a non-specific chronic inflammatory condition of the gastrointestinal tract, characterized by damage to intestinal epithelial cells (IECs) and inflammation. Mesenchymal stem cell-derived exosomes show therapeutic potential in IBD, but the underlying mechanisms remain unclear. This study investigates the therapeutic potential of bone marrow mesenchymal stem cell (BMSC)-derived exosomes and their molecular mechanism in IBD. We isolated and characterized exosomes from mouse BMSCs, confirming their typical size, morphology, and marker expression. In a dextran sulfate sodium (DSS)-induced mouse IBD model, administration of BMSC-derived exosomes alleviated disease severity, colon shortening, and histopathological damage. In LPS + ATP-stimulated IECs, BMSC-exos upregulated miR-148a-3p expression, enhanced cell viability, and suppressed pyroptosis-related proteins, including NOD-like receptor protein 3 (NLRP3), ASC, cleaved caspase-1, and the N-terminus of GSDMD (GSDMD-N), and inflammatory cytokines interleukin 1β (IL-1β), IL-18, tumor necrosis factor-α (TNF-α), and IL-6. Bioinformatics and dual-luciferase reporter assays identified E26 avian leukemia oncogene 1, 5' domain (Ets-1) as a direct target of miR-148a-3p. Ets-1 knockdown reversed the effects of miR-148a-3p inhibition on IEC pyroptosis and inflammation. In conclusion, BMSC-derived exosomes deliver miR-148a-3p to IECs, where it targets Ets-1 to suppress cellular pyroptosis and inflammatory responses, offering a novel therapeutic strategy for IBD. - Source: PubMed
Publication date: 2026/07/02
Zhang FeilongSong JiZhang YunjiaoHu HejunZhou PingXu CaixiaoZhan MeinanHou AnnaLin XiangliShen Wenjuan - Tissue fibrosis represents the common terminal pathological features of multiple chronic diseases, yet effective therapeutic agents capable of retarding fibrotic progression remain limited. This review systematically delineates the antifibrotic pharmacological profile of salidroside and elucidates its multi-target synergistic mechanisms across renal, hepatic, pulmonary, and cardiac fibrosis. Our comprehensive analysis reveals that salidroside exerts multifaceted antifibrotic effects through the integrated modulation of diverse signaling networks. Specifically, it concurrently suppresses pro-fibrotic pathways including TGF-β1/Smad, Wnt/β-catenin, and PI3K/Akt/mTOR to attenuate extracellular matrix deposition and myofibroblast activation; activates the Nrf2-Keap1 antioxidant axis and the AMPK/SIRT1/PGC-1α energy metabolism pathway to enhance mitochondrial biogenesis and scavenge reactive oxygen species; and blocks p38/JNK and NF-κB inflammatory cascades to reduce TNF-α, IL-6, and IL-1β secretion. Notably, SIRT1 serves as a central hub mediating the crosstalk between ferroptosis and autophagy via the SIRT1/PINK1 axis, while simultaneously coordinating antioxidant-anti-inflammatory amplification and bidirectional inhibition of fibrotic signaling, thereby forming positive-feedback loops that circumvent compensatory pathway activation inherent to single-target interventions. Furthermore, salidroside indirectly ameliorates fibrotic microenvironments through gut microbiota remodeling and modulation of gut-organ axis metabolites including LPS and TMAO. Despite these promising preclinical findings, the clinical translation of salidroside is constrained by poor oral bioavailability, limited organ-targeting specificity, and a paucity of large-scale clinical evidence. Collectively, these findings establish salidroside as a promising multi-target antifibrotic candidate and provide a comprehensive mechanistic framework for its development into a cross-organ precision therapeutic, while highlighting the urgent need for optimized delivery systems and rigorous clinical validation to bridge the gap between basic research and clinical application. - Source: PubMed
Publication date: 2026/07/02
Liu Ai-QianByun JongwonYu Nan NanJin Mei-HuaHan Ying-HaoLee Dong SeokLee Dong-HunSun Hu-Nan - Neuroinflammatory mechanisms have long been implicated in the pathophysiology of depression, particularly in treatment-resistant depression (TRD). Peripheral immune markers such as monocyte-to-lymphocyte ratio (MLR), neutrophil-to-lymphocyte ratio (NLR), and neutrophil-to-platelet ratio (NPR) may reflect chronic or acute immune activation and could serve as potential biomarkers for treatment response. We analyzed differential blood cell counts and inflammatory ratios (MLR, NLR, NPR), as well as interleukin-6 (IL-6) and C-reactive protein (CRP) levels, in 196 patients with severe depression. Patients were grouped into unmedicated (UDC), TRD with medication only (TRD-M), and TRD with electroconvulsive therapy (TRD-ECT), and were assessed at baseline and after four weeks. TRD patients showed significantly higher monocyte and MLR levels than non-TRD patients. Within TRD, ECT responders exhibited lower monocyte and MLR values compared to non-responders. NLR levels were significantly higher in the ECT group. A positive correlation was found between NPR changes and symptom improvement based on Beck Depression Inventory-II scores (BDI-II). Our findings suggest that TRD is associated with a chronic inflammatory profile, and that ECT may induce a shift toward acute immune activation, potentially contributing to treatment response. MLR, NLR, and NPR may serve as potential biomarkers and should be evaluated in prospective studies with larger samples and detailed immune phenotyping. - Source: PubMed
Publication date: 2026/07/02
Abo Hwach AmmarTürker Seda NurHuster FranziskaGaspert AnastasiaBastami AlborzWrasse JoanaBleich StefanFrieling HelgeNickl-Jockschat ThomasMaier Hannah BenedictineNeyazi Alexandra