Recombinant Human IL-6 (Interleukin 6)
- Known as:
- Recombinant Human Interleukin-6 (Interleukin 6)
- Catalog number:
- rhil6-25
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CDI Bioscience
- Gene target:
- Recombinant Human IL-6 (Interleukin 6)
Related genes to: Recombinant Human IL-6 (Interleukin 6)
- 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: Recombinant Human IL-6 (Interleukin 6)
Related articles to: Recombinant Human IL-6 (Interleukin 6)
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Publication date: 2026/07/04
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Publication date: 2026/07/04
Ye QiongLi JimeiJu Ying - IDH wild-type glioblastoma (IDH-wt GBM) exhibits substantial intratumoral heterogeneity, which contributes to treatment resistance, disease recurrence, and variable clinical outcomes. This study aimed to identify radiomics-based intratumoral heterogeneity (RITH) subtypes in IDH-wt GBM and to assess their prognostic relevance, associated pathomic differences, and transcriptomic associations. - Source: PubMed
Publication date: 2026/07/03
Duan XinNiu WenjuLi XuanLi ZehuiLiang QianYang XiangliTan YanZhang Hui - Inflammatory response and oxidative stress interact with each other and are involved in the pathogenesis of various chronic diseases. Senkyunolide A (SenA) is a phthalide compound isolated from the traditional Chinese medicine Chuanxiong Rhizoma (Ligusticum chuanxiong Hort.). At present, the anti‑inflammatory and anti‑oxidative stress effects of SenA remain unclear. In this study, we adopted an integrated strategy combining network pharmacology, bioinformatics analysis, molecular docking, molecular dynamics simulation, bio‑layer interferometry (BLI), and in vitro experiments to explore the anti‑inflammatory and anti‑oxidative stress effects and potential targets of SenA. Through network pharmacology and bioinformatics analysis, we identified four core target genes (Il1b, Ptgs2, Nos2, and Hmox1) of SenA against LPS‑induced inflammation in RAW264.7 cells. Direct binding of SenA to IL‑1β and PTGS2 was confirmed by molecular docking, molecular dynamics simulation, and BLI assays. In vitro experiments showed that SenA pretreatment effectively inhibited LPS‑induced inflammatory response and oxidative stress in RAW264.7 cells, as evidenced by reduced expression of pro‑inflammatory cytokines (TNF‑α, IL‑6, and IL‑1β), decreased levels of NO, ROS, and MDA, increased GSH levels, and alleviated cell swelling and mitochondrial damage. In addition, SenA pretreatment downregulated the mRNA expression levels of the core target genes Il1b, Ptgs2, Nos2, and Hmox1. In conclusion, our findings demonstrate that SenA exerts significant anti‑inflammatory and anti‑oxidative stress effects and may serve as a candidate compound for the treatment of inflammation‑related diseases. - Source: PubMed
Publication date: 2026/07/03
Liu YueYang GuangChi XiansuWang LiudingZhang YunfanLiang XiaoZhang Yunling - Inflammation critically influences mesenchymal stem cell (MSC) behavior, affecting their survival, plasticity, and immunomodulatory functions. MSC preconditioning has emerged as a promising strategy to enhance their therapeutic potential before clinical application. Among the factors capable of modulating MSC responses, selenium has gained attention due to its role in regulating inflammatory signaling. In this study, we investigated whether high-dose sodium selenite (NaSeO) preconditioning modulates MSC behavior under inflammatory stimulation and how these changes affect macrophage responses through paracrine mechanisms. MSCs were preconditioned with NaSeO in the presence or absence of lipopolysaccharide (LPS). Cellular metabolism, apoptosis, cell-cycle progression, migration, intracellular signaling, reactive oxygen species (ROS) production, and soluble mediator release were evaluated. Macrophage responses were assessed using conditioned medium from treated MSCs. NaSeO alone did not significantly affect MSC metabolic viability. However, under inflammatory conditions, NaSeO enhanced apoptotic signaling and promoted cell-cycle accumulation in S/G2/M phases. In addition, NaSeO preconditioning reduced intracellular ROS levels, attenuated NFκB and JNK activation, and altered the MSC secretory profile, increasing nitric oxide, transforming growth factor-β, and prostaglandin E2 production while decreasing IL-6 levels. Importantly, conditioned medium from preconditioned MSCs reprogrammed macrophage responses, reducing TNF-α and IL-1β production while increasing IL-1 receptor antagonist levels. These findings demonstrate that high-dose NaSeO reprograms MSCs under inflammatory stress, enhancing their anti-inflammatory paracrine activity and capacity to modulate macrophage inflammatory responses. These results identify selenium as a key regulator of MSC-mediated immunomodulation and support sodium selenite preconditioning as a strategy to optimize MSC-based therapies for inflammatory diseases. - Source: PubMed
Publication date: 2026/07/03
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