TNF-alpha ELISA
- Known as:
- TNF-a Enzyme-linked immunosorbent assay test
- Catalog number:
- kap1751
- Product Quantity:
- EUR
- Category:
- -
- Supplier:
- Diasource
- Gene target:
- TNF-alpha ELISA
Related products to: TNF-alpha ELISA
Related articles to: TNF-alpha ELISA
- This study aimed to investigate the effects of Mediterranean and Western diet models on telomere length, oxidative stress, inflammatory markers, and total hippocampal cell count in rats. - Source: PubMed
Publication date: 2026/04/19
Tilekli Mehmet MustafaAcar Tek Nilüfer - To compare the therapeutic effects of intravenous (IV) and intratracheal (IT) delivery of adipose-derived stem cells (ADSCs) in a mouse model of bleomycin (BLM)-induced idiopathic pulmonary fibrosis (IPF). - Source: PubMed
Publication date: 2026/02/28
Ng Yan-YanChiang Chen-YuNi Yung-LunShen Huan-TingLee Chien-YingLee Tai-PingSieber MartinTseng Ching-ChiTsao Thomas Chang-YaoKuan Yu-Hsiang - This study investigated the role of TGF-β-activated kinase 1 (TAK1) in synovial inflammation and hyperplasia in JIA synovial fibroblasts (JIASFs). - Source: PubMed
Publication date: 2026/04/17
Shanta Meena ALough Donavon CHenderson Lauren ANigrovic Peter AAhmed Salahuddin - The widespread use of glyphosate-based herbicides (GBHs), including formulations such as Roundup, has raised toxicological concern due to their capacity to induce oxidative stress, inflammatory signaling, and mitochondrial dysfunction leading to hepatocellular injury. The present study investigated whether coenzyme Q10 (CoQ10) confers hepatoprotection against GBH exposure through modulation of oxidative stress-driven P2X7/NLRP3 inflammasome signaling and downstream inflammatory and apoptotic pathways. Fifty male ICR mice were randomly assigned to five groups (control, sham, CoQ10, GBH, and GBH + CoQ10) and treated by oral gavage for 49 days with Roundup (500 mg/kg/day), CoQ10 (200 mg/kg/day), or their combination. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels were assessed along with hepatic oxidative stress markers malondialdehyde (MDA), glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI). Liver injury was evaluated histologically, while proliferative and inflammatory responses were analyzed by immunohistochemistry. Hepatic expression of inflammasome- and apoptosis-related genes (P2X7, NLRP3, caspase-1, IL-1β, NF-κB, TNF-α, caspase-3, and Bcl-2) was quantified by RT-qPCR. GBH exposure markedly increased serum liver enzymes, disrupted oxidative balance, and induced necroinflammatory liver injury with Kupffer cell activation and hepatocellular nuclear alterations. These changes were associated with increased PCNA and COX-2 immunoreactivity, activation of the P2X7-NLRP3 inflammasome axis, and a proapoptotic transcriptional profile. CoQ10 coadministration attenuated biochemical, histopathological, inflammatory, and apoptotic alterations, although several parameters remained incompletely normalized. In conclusion, CoQ10 provides partial but meaningful hepatoprotection against GBH-induced liver injury, highlighting P2X7-NLRP3-linked oxidative inflammation as a key mechanism in GBH hepatotoxicity. - Source: PubMed
Publication date: 2026/04/18
Mutluay DuyguYakut SedaTenekeci Gözde YücelAkı Rüveyda HilalDenk BarışKara Adem - Tramadol (TRM) is a commonly prescribed opioid analgesic; however, accumulating evidence suggests that it may exert toxic effects on vital organs, including the lungs. This study aimed to elucidate the mechanisms underlying TRM-induced lung injury and to investigate the potential protective role of rutin (RUT), a bioactive flavonoid with potent antioxidant and anti-inflammatory properties. In a rat model, lung tissues were analyzed using histopathological examination, biochemical assays for oxidative stress parameters, RT-qPCR for gene expression analysis [nuclear factor E2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), NAD(P)H:quinone acceptor oxidoreductase 1 (NQO1), nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), inducible nitric oxide synthase (iNOS), Bax, Bcl-2, and Caspase-3], and immunohistochemical (IHC) evaluation of Beclin-1 and 3-nitrotyrosine (3-NT) expression. TRM administration caused severe pulmonary structural alterations, including alveolar collapse, interalveolar septal thickening, inflammatory infiltration, edema, and hemorrhage. These histopathological changes were associated with pronounced oxidative stress, as evidenced by suppressed superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) activities, depletion of glutathione (GSH), increased lipid peroxidation, and disruption of the Nrf2/HO-1/NQO1 antioxidant signaling axis. Furthermore, TRM markedly activated endoplasmic reticulum (ER) stress responses (PERK and ATF-6), upregulated apoptotic markers (Bax and Caspase-3), downregulated Bcl-2 expression, and enhanced autophagy-related Beclin-1 immunoreactivity. In parallel, significant activation of inflammatory and nitrosative pathways was observed, characterized by elevated NF-κB, TNF-α, and iNOS expression and increased nitrotyrosine accumulation. In contrast, RUT treatment substantially ameliorated TRM-induced lung injury by restoring antioxidant capacity, suppressing ER stress-mediated apoptosis and autophagy, and attenuating inflammatory and nitrosative responses. Overall, these findings demonstrate that RUT confers significant protection against TRM-induced pulmonary toxicity through coordinated modulation of oxidative stress, ER stress, apoptosis, autophagy, and inflammation. - Source: PubMed
Publication date: 2026/04/18
Gönen Mustafa ÖnderAkaras NurhanŞimşek HasanKandemir ÖzgeCaglayan CuneytMutlu HüseyinKandemir Fatih Mehmet