Recombinant Human IL-6 (Interleukin 6)
- Known as:
- Recombinant Human Interleukin-6 (Interleukin 6)
- Catalog number:
- rhil6-5
- 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)
- Cisplatin‑induced acute kidney injury (CI‑AKI) is one of the most common comorbidities in patients undergoing chemotherapy, notably limiting the clinical use of cisplatin. However, the pathogenesis of CI‑AKI remains to be fully elucidated. Sulforaphane (SFN), a NRF2 agonist, exhibits anti‑inflammatory, antioxidant and anti‑apoptotic effects, thus SFN exerts protective effects in kidney injury diseases. However, the possible role and underlying mechanisms of SFN in CI‑AKI remain ambiguous. An model of CI‑AKI was constructed using C57BL/6 mice that were administered a single intraperitoneal cisplatin injection (20 mg/kg) and conditionally treated with SFN (10 mg/kg). Serum creatinine (Scr) and blood urea nitrogen (BUN) levels were detected by biochemical analysis. Western blotting was performed to assess the expression of renal injury markers, as well as the apoptosis‑related proteins cleaved caspase‑3, caspase‑3, Bax and Bcl‑2. Furthermore, hematoxylin and eosin and periodic acid‑Schiff staining were employed to detect renal tissue lesions in mice, and TUNEL staining was used to evaluate the apoptosis of renal tissues in each group . Immunohistochemistry was used to assess the expression of inflammatory marker F4/80 in mouse renal tissues, and ELISA was used to detect the expressions of the inflammatory markers IL)‑1β, IL‑6 and tumor necrosis factor‑α (TNF‑α) in the serum of mice in each group. DCFH‑DA) analysis was used to detect reactive oxygen species (ROS) levels and biochemical analysis was used to evaluate the expression levels of malondialdehyde, superoxide dismutase and glutathione. Finally, western blotting and immunohistochemistry were performed to evaluate the expression of NRF2. An model of CI‑AKI was constructed using HK‑2 cells induced by cisplatin (10 µg/ml) that were conditionally treated with one or both of SFN (5 µM) and the NRF2 inhibitor ML385 (1.9 µM). Reverse transcription‑quantitative PCR was performed to evaluate the expression of NRF2. Cell Counting Kit‑8 assay was performed to assess the viability of HK‑2 cells in different groups, whereas flow cytometry was used to assess the apoptosis of HK‑2 cells in different groups. DCFH‑DA analysis was performed to evaluate the expression of ROS in different treatment groups. Furthermore, ELISA was used to evaluate the expressions of IL‑1β, IL‑6 and TNF‑α in each group. SFN notably decreased the serum levels of Scr and BUN and decreased the expression levels of kidney injury molecule‑1 and neutrophil gelatinase‑associated lipocalin in the cisplatin‑induced model group. Histopathological examination revealed attenuated renal structural damage and preserved tubular architecture in the SFN intervention group. Furthermore, SFN notably inhibited the apoptosis, inflammation and oxidative stress of renal tissues induced with cisplatin. Additionally, SFN markedly upregulated NRF2. , the NRF2 inhibitor ML385 partially attenuated the effects of SFN on the viability, apoptosis, inflammation and oxidative stress of HK‑2 model cells. The present study indicated that SFN exerted its nephroprotective effect through NRF2‑mediated anti‑inflammatory, antioxidant and anti‑apoptotic mechanisms, positioning SFN as a promising therapeutic candidate for clinical management of chemotherapy‑associated kidney injury. - Source: PubMed
Publication date: 2026/06/26
Wu ZeyuLu MengtingXu LeiLuo MingShan LimeiXing HongxiaLi WenwenQian Junling - Smoking has been linked to alterations in cellular inflammatory pathways and adverse outcomes in orthopaedic procedures. It is unclear how patient smoking affects the intra-articular microenvironment in the setting of symptomatic meniscal tears. - Source: PubMed
Publication date: 2026/06/26
Kurtz Jessica LEhlers MalloryMontgomery Samuel RKaplan Daniel JStrauss Eric J - This experiment explored the impacts of potassium diformate (K-diformate) on growth performance, inflammation, intestinal barrier function, and gut microbiota in nursery piglets. Twenty-four weaned piglets were assigned to four dietary groups supplemented with 0%, 0.6%, 1.2%, or 1.8% K-diformate for 28 days. Results showed that the FCR decreased linearly with increasing K-diformate levels ( < 0.05). Importantly, piglets in the 1.8% K-diformate group had the lowest FCR, which was lower than that of the control group by 15.03% and 14.29% in weeks 1-2 and 3-4, respectively ( < 0.05). Additionally, piglets receiving 1.8% K-diformate demonstrated lower serum IL-6 levels (9.27% reduction), along with reduced jejunal IL-6 (17.64%), IL-1β (10.29%), and TNF-α levels (14.01%) relative to the control group ( < 0.05). Furthermore, piglets in the 1.8% K-diformate group exhibited decreased serum D-lactate (36.00% reduction) and LPS levels (9.90% reduction), and elevated serum GLP-2 levels (9.23% increase), as well as upregulated jejunal ZO-1, Occludin, and MUC2, both at mRNA and protein expression levels ( < 0.05). Microbiota analysis revealed piglets in the 1.8% K-diformate group exhibited higher abundances of , , , and , while showing lower abundances of , , , and ( < 0.05). Correlation analysis further revealed associations between , , , and with inflammation, and between , , , , and with intestinal barrier function ( < 0.05). Collectively, dietary addition with K-diformate (especially 1.8%) improved growth performance, inflammation, and intestinal barrier function associated with gut microbiota modulation in nursery piglets. - Source: PubMed
Publication date: 2026/06/24
Zou TiandeZhang LinaLi QinCheng YongLu LiZhong SongtaoQu MingrenChen Jun - Background Oral squamous cell carcinoma (OSCC) is a common malignancy with variable clinical outcomes and a high risk of recurrence. Conventional prognostic indicators often fail to fully capture tumor behavior. Serum growth factors and inflammatory mediators, such as the epidermal growth factor receptor (EGFR), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α), may provide additional insights into disease progression and prognosis. This study aimed to evaluate the prognostic significance of serial serum levels of EGFR, IL-6, and TNF-α in patients with OSCC. Methodology This prospective cohort study included 120 patients with histopathologically confirmed OSCC. Serum samples were collected at baseline, 6 months, and 12 months and analyzed for EGFR, IL-6, and TNF-α using enzyme-linked immunosorbent assay. Clinical and pathological data were also recorded. Statistical analyses were performed. Intergroup comparisons were conducted using independent t-tests, correlations were assessed using Spearman's coefficient, and Cox proportional hazards regression analysis was used to identify predictors of recurrence-free survival. Results In total, 34 (28.33%) patients with recurrence showed significantly higher baseline levels of EGFR (82.3 ± 24.1 vs. 62.9 ± 19.4 ng/mL), IL-6 (26.4 ± 10.8 vs. 15.9 ± 7.1 pg/mL), and TNF-α (42.7 ± 16.3 vs. 28.6 ± 12.1 pg/mL) compared to non-recurrent cases (p < 0.001). Similar trends persisted at 6 and 12 months (p < 0.001). Significant positive correlations were identified between baseline biomarker levels and clinicopathological parameters. Tumor size showed moderate correlations with EGFR (r = 0.54), IL-6 (r = 0.48), and TNF-α (r = 0.42). Similarly, tumor-node-metastasis stage demonstrated strong correlations with EGFR (r = 0.61), IL-6 (r = 0.57), and TNF-α (r = 0.51). Lymph node metastasis also showed significant positive correlations with EGFR (r = 0.52), IL-6 (r = 0.49), and TNF-α (r = 0.45) (p < 0.001). Multivariate analysis identified the baseline EGFR (p < 0.001), IL-6 (p = 0.002), and TNF-α (p = 0.028) as independent predictors of recurrence of OSCC. Conclusions Serum EGFR, IL-6, and TNF-α may serve as potential prognostic indicators for OSCC. The findings of this study suggest that combining growth factors and inflammatory biomarkers could have clinical utility for improving prognostic assessment in OSCC. Serial monitoring may provide a dynamic approach for identifying patients at higher risk of recurrence, thereby facilitating timely therapeutic interventions and closer surveillance. Incorporation of these markers into routine clinical protocols might contribute to more personalized treatment strategies and potentially improve long-term outcomes. However, further large-scale studies are required to validate these findings and establish standardized clinical thresholds. - Source: PubMed
Publication date: 2026/05/25
Patil TejalKalsi JasmineKumar MukeshTiwari Rahul VcRemesh AmbiliAppilly Unni J - Vitreoretinal lymphoma (VRL) is a rare, high-grade B-cell lymphoma that affects immune-privileged sites and is classified as a variant of primary central nervous system lymphoma (PCNSL). The pathogenesis of VRL, including the origin of malignant B-cells, remains poorly understood. Cytokines, chemokines, and growth factors are thought to play critical roles in both the homing and autocrine proliferation of lymphomatous B-cells. In this study, we present the first longitudinal analysis of the dynamic interplay of vitreous immune mediators during intravitreal (IVT) methotrexate and dexamethasone therapy in a patient with VRL. - Source: PubMed
Publication date: 2026/06/10
Saturno Maria CarmelaIannetta DaniloLambiase Alessandrode Smet Marc D