ELISA Mouse , TNF-alpha
- Known as:
- Enzyme-linked immunosorbent assay test Mouse , TNF-a
- Catalog number:
- RBMS607/2R
- Product Quantity:
- 96 wells (1 kit)
- Category:
- -
- Supplier:
- Biovend
- Gene target:
- ELISA Mouse TNF-alpha
Related products to: ELISA Mouse , TNF-alpha
Related articles to: ELISA Mouse , TNF-alpha
- In this work, Eucalyptus salubris seeds extract (ESS) was characterized using liquid chromatography (LC) coupled to mass spectrometry (MS), and its in vitro and in vivo anti-inflammatory properties were evaluated. Through LC-MS and MS analysis, flavanonols and monounsaturated fatty acids were found to be the most abundant components, while unreported galloylated flavanonols were profiled. ESS attenuated the denaturation of Bovine Serum Albumin (BSA), significantly stabilized rats Red Blood Cells (RBC) membranes, and inhibited both Cyclooxygenase-1 (COX-1) and Cyclooxygenase-2 (COX-2) enzymes, indicating its ability to reduce inflammation. The in vivo study showed that ESS significantly reduced the carrageenan-induced paw edema in rats and normalized the inflammatory cytokines Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-6 (IL-6) levels. In addition, ESS alleviated formaldehyde-induced arthritis symptoms through a remarkable reduction in oxidative stress biomarkers (evidenced by decreased Malondialdehyde (MDA), Glutathione (GSH), and Nitric Oxide (NO) levels, along with increased Superoxide Dismutase (SOD) and Catalase (CAT) activities), as well as the restoration of the hematological profile (reduction in white blood cell (WBC) count and erythrocyte sedimentation rate (ESR), accompanied by an increase in red blood cell (RBC) count and hemoglobin (Hb) levels). These effects are largely attributable to the richness of ESS in phenolic compounds, flavonoids, and other bioactive secondary metabolites. Collectively, these findings supported the therapeutic potential of E. salubris extract as a natural source of anti-inflammatory and antioxidant agents, warranting further investigation for potential pharmaceutical or nutraceutical applications. - Source: PubMed
Publication date: 2026/04/22
Ferjani NouhaMekky Reham HassanContreras María Del MarJalouli MarouaFeriani AnouarTir MeriamSaadaoui EzzeddineHarrath Abdel HalimTlili Nizar - Mitochondrial dysfunction, oxidative stress, and neuroinflammation play a critical role in the occurrence and progression of Alzheimer's disease (AD). MicroRNAs (miRNAs) have been studied recently as potential therapeutic approaches for AD. In this study, we examined the function and underlying mechanism of microRNA-25802 (miR-25802), a newly discovered miRNA in an AD model. In order to evaluate the levels of oxidative stress, mitochondrial damage and neuroinflammation in neuroblastoma cells, four experimental groups were created: control group (neuroblastoma cells, SH-SY5Y), amyloid beta (Aβ)-induced neuroblastoma cells (SY5Y-Aβ), small extracellular vesicles (sEVs)-only group and miR-25802-loaded small extracellular vesicles (sEV-miR25802) administered group. Neuroinflammation, oxidative stress, mitochondrial damage, tau hyperphosphorylation, and Aβ accumulation were evaluated in Aβ-induced neuroblastoma cells. Oxidative stress was analyzed by measuring reactive oxygen species (ROS), malondialdehyde (MDA), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase 1 (GPX1). Inflammatory markers such as tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecule 1 (ICAM1), and brain-derived neurotrophic factor (BDNF) mRNA levels, a neurotrophic factor, were evaluated by RT-qPCR. Neurofilament light chain (NfL), vascular endothelial growth factor-A (VEGF-A), macrophage migration inhibitory factor (MIF), monocyte chemoattractant protein-1 (MCP-1) and cytochrome c (Cyt-c), mitochondrial transcription factor A (TFAM), PTEN-induced kinase 1 (PINK1) and dynamin-1-like protein (DNM1L) protein levels were determined by ELISA. Mechanistically, sEV-miR25802 were shown to provide anti-inflammatory and neuroprotective effects by regulating neuroinflammation, mitochondrial dysfunction, and oxidative stress. These findings reveal the regulatory role of miR-25802 on neuroinflammation, mitochondrial damage, and oxidative stress and suggest that it may be a potential therapeutic target for AD. - Source: PubMed
Publication date: 2026/04/23
Çelik HamitDalkılınç ElifAydın ŞeymaÇelik OğuzKüçükler SefaTopal AhmetAkay RamazanGönüllü SinanYıldız Mustafa OnurAlım BülentÖzdemir Selçuk - - Source: PubMed
Publication date: 2026/04/23
Poniatowski Łukasz AKwiatkowska MagdalenaSiwińska AgnieszkaAcewicz AlbertOlczak Mieszko - Liver fibrosis represents an abnormal wound-healing response to chronic hepatic injury. It is characterized by the excessive production and deposition of extracellular matrix components, ultimately resulting in the formation of a fibrotic scar. Visnagin, a phytochemical, has antioxidants and anti-inflammatory activity and modulates apoptosis; however, the role of visnagin in liver fibrosis has not been previously explored. Herein, we have induced liver fibrosis using thioacetamide (TAA; 200 mg/kg) through the intraperitoneal (i.p.) route every third day for 8 weeks in Sprague Dawley rats. Visnagin (5 and 10 mg/kg) co-treatment was given via the i.p. route every day for 8 weeks. At the end of the visnagin intervention, various biochemical, oxidative stress parameters, histopathological assessments, and quantitative reverse-transcription polymerase chain reaction (qRT-PCR) analyses were performed. Visnagin administration resulted in a significant decrease in the liver-to-body weight ratio and liver injury markers, including alanine transaminase, aspartate aminotransferase, and alkaline phosphatase. Additionally, visnagin attenuated TAA-induced oxidative stress by restoring levels of malondialdehyde, nitrite, and superoxide dismutase. Histopathological assessments confirmed the hepatoprotective effects of visnagin against TAA-induced liver injury, as evidenced by a reduction in hepatocyte damage and collagen deposition. Further, at a molecular level, visnagin treatment reduces the expression of caspase-3 and genes related to inflammation (TLR4, TNF-α, IL-6, NLRP3) and fibrosis (α-SMA, Col1A1, TGF-β, MMP9, and TIMP1) in TAA-treated rats. - Source: PubMed
Publication date: 2026/04/22
Goswami YogenderYadav PoonamSingh Sumeet KumarNavghare Akshay AmrutaRajput SonuKhurana AmitBhatti Jasvinder SinghNavik Umashanker - Escherichia coli (E. coli) is a leading cause of invasive bacterial infections in humans. Pathogenic E. coli is not only the major etiological agent of enteric/diarrheal disease and urinary tract infections, but also among the most common causes of sepsis and meningitis. Caspase-8 is known to regulate apoptotic and pyroptotic cell death in response to bacterial and viral infections. Here we demonstrate that caspase-8 plays a critical role in E. coli-induced macrophage apoptosis in vitro and in regulating immune response and host death in vivo. Incubation of mouse bone marrow derived macrophages (BMDMs) with an E. coli K1 strain CE10 triggered robust cell death, which is independent of the NAIP/NLRC4/caspase-1/GSDMD pathway. CE10 stimulation induced caspase-8 activation, and macrophages deficient in caspase-8 and RIPK3, but not RIPK3 alone, were protected from CE10-induced cell death. In an intraperitoneal injection sepsis model, E. coli-induced IL-1β, TNF-α, and IL-6 production was markedly reduced in caspase-8-/-/RIPK3-/- mice, compared with RIPK3-/- or wild type mice. Accordingly, the survival rate was significantly improved in caspase-8-/-/RIPK3-/- mice. Moreover, caspase-8 deficiency attenuated CE10-induced NF-κB activation and cytokine production in BMDMs. Together, our findings identify caspase-8 as a central mediator of E. coli-induced cell death, immune response, and establish its critical contribution to host mortality during E. coli infection. - Source: PubMed
Chai ZhuodongZhou YuqiYang LingZhang YanHossain SukriaZhang GuoyingQi JiaqianZhang ZiranShiroishi ToshihikoWei YinanLi Zhenyu