Human TNF_alpha 1 mg
- Known as:
- Human TNF_alpha 1 mg
- Catalog number:
- 1050-1000
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- Human TNF_alpha 1
Related products to: Human TNF_alpha 1 mg
Related articles to: Human TNF_alpha 1 mg
- Allergic conjunctivitis (AC) is an IgE-mediated type I hypersensitivity disorder characterized by conjunctival hyperemia, itching, and increased tear secretions. This study aims to investigate the mechanism of FOXP3 in the inflammatory activation of human conjunctival epithelial cells (HConEpiCs) in AC. Serum samples were collected from AC patients and healthy volunteers for correlation analysis of FOXP3 with inflammatory cytokines (IL-6/IL-8/TNF-α/CRP) and immunoglobulins (IgG/IgA/IgE). FOXP3, KAT5, and PDCD4 expression were measured by RT-qPCR, followed by Pearson correlation analysis. HConEpiCs were used to establish an AC cell model, followed by assessment of cell viability and inflammatory cytokines (IL-6/IL-8/TNF-α/IL-10/IL-4). The binding of FOXP3 to the KAT5 promoter and KAT5 and H3K27ac enrichment on the PDCD4 promoter were detected. FOXP3 expression was downregulated in AC patient, while KAT5 and PDCD4 were upregulated. FOXP3 negatively correlated with IL-6, IL-8, TNF-α, C-reactive protein, serum IgG, IgA, IgE, and eosinophil ratio. In histamine-stimulated HConEpiCs, FOXP3 overexpression inhibited inflammation. Mechanistically, FOXP3 bound to the KAT5 promoter to inhibit KAT5 expression, reduced KAT5 and H3K27ac enrichment on the PDCD4 promoter, and downregulated PDCD4 expression. KAT5 or PDCD4 overexpression reversed FOXP3-mediated inhibition of HConEpiC inflammatory activation. In conclusion, FOXP3 overexpression attenuates inflammatory activation of HConEpiCs by inhibiting KAT5 expression and reducing KAT5/H3K27ac-mediated PDCD4 transcription. - Source: PubMed
Publication date: 2025/09/17
Deng Zifeng - Myristoylated alanine-rich C kinase substrate (MARCKS) is a versatile unstructured protein involved in numerous cellular processes and associated with various diseases. In this study, the effect of MARCKS' N-terminal sequence-derived inhibitor peptides MANS ("myristoylated N-terminal sequence") and BIO-11006 on monocytic ROS production and migration was assessed. - Source: PubMed
Publication date: 2025/09/17
Kühl FriederikeKopper Jana LeaWriede Lena SofieWelz BastianLichtinghagen RalfBrand KorbinianHuber René - Rheumatoid arthritis (RA) is a chronic autoimmune disease characterised by inflammation in the synovial lining of joints, leading to pain, stiffness, and significant functional limitations. Current treatments focus on managing symptoms and slowing disease progression, but they often have side effects and may not be effective for all patients. This study investigated the effects of alpha-lipoic acid (ALA) on immune response and inflammation in mouse model of arthritis. Adjuvant-induced arthritis (AIA) was established in mice, and ALA was administered to mice at a dose of 75 mg/kg via oral gavage twice daily for 7 consecutive days. ALA administration significantly reduced arthritis severity, as evidenced by decreased paw oedema and arthritis score. ALA treatment led to a significant reduction in plasma levels of IL-17A, TNF-α, and MMP-3, key biomarkers of arthritis disease activity. ALA decreased the number of circulating Th17 and NF-κB p65 CD4 T lymphocytes, suggesting its potential to modulate the immune response. ALA downregulated the expression of pro-inflammatory genes (IL17F, TNF) and upregulated the expression of the anti-inflammatory cytokine IL10 gene in the joint tissues. In the joint tissue, ALA modulated the expression of NFKB1, STAT3, GATA3, TBX21, and RORC, all of which are key transcription factors associated with arthritis pathogenesis. Molecular docking results suggest potential binding interactions between ALA and key molecules like GATA-3 and TNF-α, as a potential mechanism for its anti-inflammatory properties. These findings support ALA's potential as a promising therapeutic agent for RA in human patients, as it appears to modulate inflammation, immune responses, and key molecular pathways involved in disease pathogenesis. - Source: PubMed
Publication date: 2025/09/17
Aboelenin Mohamad MHefnawy MohamedEmran Talha BinShafey Heba IZoheir Khairy M A - Ulcerative colitis (UC) is a chronic autoimmune inflammatory condition distinguished by tissue damage in colonic mucosal layers. Several pro-inflammatory cytokines are involved in the immunopathogenesis of UC. Multiple studies showed that Toll-like receptor 4 (TLR4) expression markedly increases in UC patients. Thus, concentrating on this pathway may serve as the foundation for novel drug development targeting for treating or impeding the progression of UC. This study aims to explore the effects of pirfenidone (PRF) versus dexamethasone (DEX) on oxidative stress, tissue injury, inflammation, and fibrosis in a rat model of colitis using both biochemical and histopathological analysis. Colitis was induced by administering a single dose of 3% acetic acid (AA) intrarectally. Control animals received injections of an equivalent volume of 0.9% NaCl. Rats were then treated with either 14 days of DEX (2 mg/kg /day; p.o.) or PRF (100 mg/kg/day; p.o.). Animals were sacrificed on day 21 (7 days for acclimatization + 14 days for treatment), and then, the distal 10 cm of each colon was excised. Subsequently, all tissue samples were assessed for macroscopic damage, pathological findings, and different biochemical markers. Both drugs significantly suppressed the elevated levels of inflammatory markers, including TLR4, IL-1β, myeloid differentiation primary response protein 88 (MyD88), Bcl-2-associated X protein (BAX), nuclear factor kappa (NF-κB), tumor necrosis factor-alpha (TNF-α), microRNA-146a (miR-146a), caspase-3, transforming growth factor-beta (TGF-β), connective tissue growth factor (CTGF), and myeloperoxidase (MPO), compared to the untreated UC Group. Additionally, they significantly elevated B-cell lymphoma 2 (BCL2) and platelet-derived growth factor (PDGF) levels, indicating their potential to mitigate inflammation and promote tissue repair. Histologically, PRF and DEX preserved intestinal structure as compared to the control group. PRF is considered a promising and effective anti-inflammatory alternative in the management of rat models of acetic acid-induced colitis. - Source: PubMed
Publication date: 2025/09/17
Wanas HanaaMekawy Dina MRaafat Hamed Reham MEid Ragaey AhmadAbd Elmaogod Eman AMusa Eid N AliAllam Mohamed A MAttia Abdelrahman MGalal Amr M - Glial cells play a critical role in shaping the tumor microenvironment in brain metastases, facilitating disease progression through complex tumor-glial cell and distinct glia-to-glia signaling pathways. To investigate these interactions, we performed RNA sequencing of astrocytes, microglia, and oligodendrocytes at various stages of brain metastatic progression, combined with spatial transcriptomics and cell-cell crosstalk analysis. Glial cells not only converged on tumor-promoting pathways such as RAS and Gap junction signaling in tumor cells but also engaged in distinct autocrine and paracrine signaling critical for inter-glial communication. Unique ligand-receptor pairs, including OSM-OSMR, CCL4-CCR5, CXCL16-CXCR6, IL1A/B-IL1R, and TNF-TNFR, functioned as key drivers of inter-glial crosstalk, which sustained the tumor-supportive niche. Therapeutic targeting of CCL4-CCR5 signaling with maraviroc, an FDA-approved antiviral drug, significantly reduced brain metastasis progression without exerting direct cytotoxic effects on tumor cells. These findings highlight a promising therapeutic strategy that focuses on modulating glial communication within the tumor microenvironment. By disrupting the supportive glial niche rather than targeting tumor cells directly, this represents a distinct and potentially less toxic approach for managing brain metastases. - Source: PubMed
Publication date: 2025/09/16
Ahn Ju YoungDong WenjuanPuri AkshjotVasquez MatthewRaghunathan RakshaYang LiSheng JiantingZhao HongWong Stephen T C