Human Cellexp Human Recombinant IL-17A proteins
- Known as:
- Human Cellexp Human Recombinant Interleukin-17A proteins
- Catalog number:
- 6468-10
- Product Quantity:
- 10
- Category:
- Proteins
- Supplier:
- Biovis
- Gene target:
- Human Cellexp Recombinant IL-17A proteins
Related genes to: Human Cellexp Human Recombinant IL-17A proteins
- Gene:
- IL17A NIH gene
- Name:
- interleukin 17A
- Previous symbol:
- CTLA8, IL17
- Synonyms:
- IL-17A, IL-17
- Chromosome:
- 6p12.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-10-25
- Date modifiied:
- 2019-04-23
Related products to: Human Cellexp Human Recombinant IL-17A proteins
Related articles to: Human Cellexp Human Recombinant IL-17A proteins
- 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 - Zinc oxide (ZnO) has been used at pharmacological levels to promote gut health and growth performance in the critical postweaning (PW) phase of piglets. The pharmacological use of ZnO in piglet diets has been banned in Europe and other countries due to antimicrobial resistance and environmental concerns. Therefore, understanding its mode of action, including its molecular mechanisms, is crucial for developing effective and sustainable alternatives. We investigated the mechanisms by which dietary supplementation with 3,000 mg/kg ZnO supports gut health and improves growth performance of piglets during the first 14 days PW. During the 2 weeks of trial (0-14 d PW), ZnO fed piglets had higher average daily gain (165 vs. 123 g/d; < 0.01), and tended to have increased average daily feed intake (204 vs. 181 g/d; < 0.1) and improved gain-to-feed ratio (0.669 vs. 0.774; < 0.05) compared to control piglets. Feces from piglets in the ZnO group were also more consistent during the 2 weeks of trial ( < 0.01). At day 14 PW, ZnO piglets had lower calprotectin concentrations in serum ( < 0.01). Dietary ZnO downregulated several genes, involved in immune, oxidative and inflammatory responses, in jejunal (, , , and ) and ileal (, , , and ) mucosa ( < 0.05). It also downregulated the expression of the zinc transporter , that is associated with zinc homeostasis, in both tissues. Notably, which promotes energy production and lipid metabolism through fatty acid oxidation, was upregulated by ZnO in ileum. In conclusion, the current results suggest that high dietary levels of ZnO reduce the expression of inflammatory cytokines, the oxidative enzyme , pathogen recognition proteins, and zinc transporters while promoting the expression of gene related with energy metabolism in the intestine. Therefore, ZnO can facilitate a smoother weaning transition to reduce weaning related gut health disturbances, ultimately contributing to gut homeostasis and improved performance. - Source: PubMed
Publication date: 2025/09/01
Ng'ang'a Zacharia WaithakaTous NuriaBallester MariaLeskovec JakobJimenez-Moya BeatrizBeltrán-Debón RaúlTorrallardona DavidTarradas Joan - Vascular calcification (VC), characterized by pathological calcium deposition in arterial walls, is a major contributor to cardiovascular morbidity in chronic inflammatory diseases such as atherosclerosis, chronic kidney disease (CKD), and diabetes. Emerging evidence underscores the pivotal role of interleukin (IL) family cytokines in modulating VC through dual pro- and anti-calcific mechanisms. Pro-inflammatory IL members, including IL-1β, IL-6, IL-17A, and IL-29, drive osteogenic transdifferentiation of vascular smooth muscle cells (VSMCs) by activating pathways such as NF-κB, STAT3, NLRP3 inflammasomes, and Wnt/β-catenin. These pathways upregulate osteogenic markers (e.g., Runx2, BMP-2) and promote oxidative stress, matrix remodeling, and pyroptosis. Conversely, anti-inflammatory cytokines like IL-10 counteract calcification by suppressing inflammatory signaling, enhancing autophagy, and restoring mineral homeostasis. This review highlights the dynamic interplay between IL cytokines, metabolic dysregulation, and epigenetic modifications in VC pathogenesis. It advocates for multi-target approaches, such as combining TYK2/STAT3 inhibition with metabolic reprogramming, to disrupt pathological crosstalk. Future research must address spatiotemporal heterogeneity in IL signaling and optimize therapeutic specificity to translate mechanistic insights into clinical applications. Harnessing the IL family's dual roles offers transformative potential for mitigating VC while preserving immune integrity. - Source: PubMed
Publication date: 2025/09/01
Zhao YikunLi HengGuo Yuanyuan - The pathogenesis of cholestatic liver disease (CLD) is unknown, but the influence of gut microbiota and inflammation cannot be ignored. In this study, we attempted to provide theoretical insights for the diagnosis and treatment of CLD in children by analysing the association between gut microbiota, IL-17 levels and clinical characteristics. This research involved 21 children diagnosed with CLD and 11 healthy controls. Blood and faecal samples were collected from these participants. Blood samples underwent analysis for clinical indicators and IL-17 concentrations. Gut microbiota was examined through 16S rRNA gene sequencing for identification and functional prediction. A positive correlation between IL-17 levels and clinical parameters (total bile acids, alanine aminotransferase, aspartate aminotransferase and triglycerides) in children with CLD was observed. Notably, children with CLD exhibited reduced diversity and disturbances in gut microbiota, highlighted by a severe decrease of (genus ). Moreover, increased relative abundance of secondary bile acid-promoting (e.g. , and ) and deleterious (e.g. and ) flora in the intestinal flora of children with CLD was positively correlated with IL-17, leading to increased inflammation and CLD aggravation. Functional predictions of gut microbiota revealed higher concentrations of l-asparagine transporter, ABC-type polar amino acid transport system and glycolysis II (from fructose 6-phosphate) functions, while the function of the Na-driven multidrug efflux pump was decreased. In conclusion, children suffering from CLD exhibit significant gut microbiota disturbances, particularly a severe decrease in (genus ). Dysbiosis of the gut microbiota and elevated levels of IL-17 mutually reinforce each other, together mediating the onset and progression of CLD. - Source: PubMed
He Shu-LiLi Zhuo-HengLi JuanLi Ying - Xiaoqinglong Decoction (XQLD) is a traditional oriental medicine. Modified- Xiaoqinglong Decoction (M-XQLD) was established by adding astragalus membranaceus and codonopsis pilosula on the basis of XQLD. M-XQLD has been shown to be effective in therapying asthma in clinical trials, but the mechanism of M-XQLD in asthma is currently unknown. - Source: PubMed
Publication date: 2025/09/16
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