Recombinant Human IL-6
- Known as:
- Recombinant Human Interleukin-6
- Catalog number:
- SJB07-01
- Product Quantity:
- 10μg/vial
- Category:
- -
- Supplier:
- Cytokin.
- Gene target:
- Recombinant Human IL-6
Related genes to: Recombinant Human IL-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
Related articles to: Recombinant Human IL-6
- Zaleya pentandra L. (Aizoaceae) is traditionally used to treat various ailments including inflammatory conditions, but the literature is scant regarding its role in chronic inflammation. Therefore, the current study aimed to provide evidence and mechanistic understanding of extracts of the plant in chronic inflammatory conditions. - Source: PubMed
Publication date: 2026/05/22
Shafi AyeshaShehzadi NaureenHussain KhalidSaleem MuhammadRasool FatimaGul Mubashara - Neurodegenerative diseases are increasingly associated with the convergence of oxidative, inflammatory, and glycation-associated stress pathways. The present study evaluated the stress-modulatory activity and probiotic-related characteristics of Pediococcus pentosaceus TAP041, a lactic acid bacterium isolated from citrus fruit. cell-free supernatant from P. pentosaceus TAP041 (TAP041 CFS) was assessed in in vitro models of neuronal and glial stress. In SH-SY5Y neuroblastoma cells, TAP041 CFS was associated with improved cell viability, reduced intracellular ROS accumulation, a lower Bax/Bcl-2 mRNA ratio, and increased BDNF and TH mRNA expression under methylglyoxal (MGO)- and lipopolysaccharide (LPS)-induced stress. The protective effects under N-(carboxymethyl)-lysine (CML) exposure were comparatively limited, with partial modulation of apoptosis-related markers in the absence of significant viability recovery. In primary rat glial cells, TAP041 CFS attenuated LPS-induced GFAP immunoreactivity and suppressed IL-6 and TNF-α expression at the transcriptional level. TAP041 CFS also exhibited ABTS radical scavenging activity, providing direct biochemical evidence for secreted antioxidant constituents. The strain demonstrated gastrointestinal stress tolerance, intestinal adhesion capacity, and a favourable safety profile, including non-hemolytic and non-cytotoxic phenotypes, absence of transferable antibiotic resistance determinants, and no known virulence factors. whole-genome sequencing identified predicted pathways for glyoxalase-mediated detoxification, antioxidant defence, and B-vitamin biosynthesis, consistent with but not directly establishing the observed phenotypes. These findings identify P. pentosaceus TAP041 as a candidate strain warranting further investigation and provide a basis for future mechanistic and in vivo studies on probiotic-derived metabolites in neurodegeneration-related stress. KEY POINTS: • TAP041 CFS reduced ROS, normalized Bax/Bcl-2, and suppressed glial inflammation. • TAP041 exhibits probiotic potential with GI tolerance, adhesion, and a safe profile. • Genome predicts glyoxalase and antioxidant pathways; ABTS confirms CFS antioxidants. - Source: PubMed
Publication date: 2026/05/22
Jeong HuijinJang Young SeoLee ChaeeunChoi Hak-JongPark Young-Seo - Childhood maltreatment (CM) increases the risk of lifelong mental illness, yet the underlying biochemical mechanisms remain unclear. Oxidative stress (OS), alongside inflammation, may contribute to this link. This study examined whether OS mediates the link between CM and mental health in a highly vulnerable group of formerly out-of-home placed young adults and explored associations between OS and inflammatory markers. Data were collected from 131 participants (31% women, M age = 26.29 ± 3.5 years) with histories of youth residential care. CM was assessed using the Childhood Trauma Questionnaire (CTQ), and mental health via the Achenbach System of Empirically Based Assessment (ASEBA). Biomarkers of OS (Superoxide Dismutase [SOD], Glutathione Peroxidase/Glutathione Reductase ratio [GPx/GRed]) and inflammation (Interleukin-1 Receptor Antagonist [IL-1RA], Interleukin-6 [IL-6], Interleukin-10 [IL-10], C-Reactive Protein [CRP], Tumor Necrosis Factor [TNF𝛼]) were analyzed. Multiple regression models examined associations among CM, OS, inflammation, and mental health, adjusting for covariates. Greater CM exposure was associated with poorer mental health (b = 0.34, p < .001). Initial analyses indicated that GPx/GRed (b = 0.20, p = .04), -but not SOD- was related to CM, particularly emotional abuse (b = 0.21, p = .03). However, this association did not remain significant after adjusting for medication use, suggesting that medication may confound links between CM and redox biology. TNF𝛼 predicted current mental health problems (b = 0.22, p = .02), and OS and inflammatory markers were significantly interrelated. Neither OS nor inflammation mediated the CM-mental health relationship. These findings highlight a complex interplay between CM, OS, and inflammation in young adults with histories of residential care. They underscore the importance of considering medication effects when studying redox mechanisms and indicate that further research is needed to clarify the biological pathways linking CM to long-term mental health outcomes. - Source: PubMed
Publication date: 2026/05/22
von Wendorff ClaraMeier MariaDwir DaniellaGiangreco BasilioKlauser PaulDemirkiran GizemSchneider PatriciaDas Neves MickaëlBürgin DavidBoonmann CyrilFegert JörgSchmid MarcClemens Vera - Infectious diseases exacerbate atherosclerosis-associated morbidity and mortality by inducing sustained inflammatory responses characterized by elevated IL-6, TNF-α, IFN-γ, and CXCL10. Persistent CXCL10-driven recruitment of CXCR3⁺ immune cells promotes endothelial dysfunction and atherosclerotic progression. Although mesenchymal stem cells (MSCs) respond to inflammatory cues and secrete CXCL10, the contribution of CXCL10/CXCR3 signaling to intrinsic MSC immunomodulatory programming remains poorly understood. The objective of this study is to investigate whether CXCL10 signaling can modulate MSC-mediated immunoregulation. To address this, Wharton's jelly-derived MSCs (WJ-MSCs) were genetically engineered to express a membrane-anchored CXCL10-Lactadherin C1/C2 fusion protein (CXCL10-LACTC1/C2). This strategy was designed to recapitulate physiological, localized, and sustained CXCL10 signaling, enabling spatially restricted chemokine presentation that more closely mimics cell-associated CXCL10 in inflammatory microenvironments compared with soluble CXCL10. The Lactadherin C1/C2 domain was selected to achieve stable, physiological membrane anchoring without introducing artificial transmembrane domains or compromising CXCL10 bioactivity. CXCL10-LACTC1/C2-expressing MSCs exhibited increased expression of key immunoregulatory mediators, including IDO1, TGF-β1, and IL4I1. Furthermore, conditioned medium derived from these MSCs attenuated TNF-α-induced inflammatory responses in human umbilical vein endothelial cells (HUVECs), as indicated by the modulation of endothelial activation and homeostasis markers (ICAM-1, PECAM-1, KDR, vWF, and NRF2) and improvement of cell viability. Collectively, these findings provide mechanistic insight into CXCL10-mediated MSC immunoregulation and support further investigation of MSC-based and cell-free therapeutic strategies aimed at mitigating CXCL10-driven endothelial inflammation in infection-associated vascular injury and atherosclerotic disease progression. - Source: PubMed
Publication date: 2026/05/22
Molo KayaEge RukenAti̇k KübraÇıtak ElifÇulcuoğlu OrçunDarıcı HakanOrdu Emel - Periodontitis is a chronic inflammatory disease characterized by progressive alveolar bone destruction and represents a major cause of tooth loss. It has also been associated with systemic inflammatory conditions such as diabetes. Circadian rhythms, governed by clock genes, are essential for maintaining physiological homeostasis across various tissues. Circadian rhythm disruption, such as that caused by night shift work, has been associated with severe periodontitis; however, the underlying mechanisms remain incompletely understood. Period 2 (Per2), a core peripheral clock gene expressed in periodontal tissues, was investigated for its role in inflammatory bone loss under circadian disruption. In a murine ligature model, circadian disruption exacerbated alveolar bone loss, while Per2 deficiency amplified inflammatory responses. Consistently, PER2 knockdown in TNF-α-stimulated human periodontal ligament cells (hPDLCs) led to increased expression of pro-inflammatory cytokines IL-1β and IL-6. Interestingly, Per2 knockout also led to increased basal bone mass compared with wild-type mice. Mechanistically, we found miR-21, a PER2-regulated microRNA, displayed rhythmic expression in hPDLCs and was downregulated following PER2 knockdown. Further investigation demonstrated that the PER2/miR-21 axis negatively regulates osteogenic differentiation under non-inflammatory conditions via TGF-β/SMAD signaling, while under inflammatory conditions, its downregulation failed to suppress PDCD4/NF-κB signaling, resulting in elevated pro-inflammatory cytokine secretion. Finally, local delivery of miR-21 agomir significantly promoted bone recovery after ligature removal. Together, these findings identify PER2 as a key circadian regulator of inflammation-associated bone homeostasis and highlight miR-21 as a potential therapeutic target for bone regeneration in periodontitis. - Source: PubMed
Publication date: 2026/05/22
Li ShiyuZhu JingxianLiu NiankeWang XinLi YangChen QingYin WeiSong Yaling