Mouse TNF_alpha ELISPOT kit
- Known as:
- Mouse TNF_alpha ELISPOT reagent
- Catalog number:
- CT322-PR2
- Product Quantity:
- 2-plate
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- Mouse TNF_alpha ELISPOT kit
Related products to: Mouse TNF_alpha ELISPOT kit
Related articles to: Mouse TNF_alpha ELISPOT kit
- Cerebral ischemia and reperfusion induce profound mitochondrial dysfunction in neurons, characterized by excessive mitochondrial fragmentation and persistent accumulation of damaged organelles, which in turn sustain and amplify oxidative stress and inflammatory signaling. Therefore, restoring mitochondrial quality control by enhancing mitophagy to selectively eliminate dysfunctional mitochondria and maintain energy homeostasis represents a promising strategy for alleviating secondary neuronal injury. Here, we develop a phosphatidylcholine (PC)-based supramolecular self-assembly scaffold co-loaded with curcumin (Cur) and 3--butylphthalide (NBP) as therapeutic cargos. Hydrophobic interactions and π-π stacking drove the co-incorporation of both drugs into the PC scaffold, resulting in the formation of a stable supramolecular nanoagent (CNP). In neurons subjected to oxygen-glucose deprivation followed by reoxygenation (OGD/R), CNP significantly enhanced intracellular delivery, reduced reactive oxygen species levels, preserved mitochondrial membrane potential, and restored ATP production. Moreover, CNP modulated PINK1/Parkin-associated mitophagy signaling, reduced the accumulation of TOM20 and p62, and suppressed the production of IL-6 and TNF-α. In a transient middle cerebral artery occlusion and reperfusion mouse model (tMCAO/R), intravenous administration of CNP enhanced brain accumulation, reduced infarct volume, and improved neurological scores. These effects were accompanied by reduced CD86-positive pro-inflammatory microglia and increased CD31-positive vascular structures and TUJ1-positive neuronal signals. Overall, CNP represents a promising dual-drug nanoagent strategy for neuroprotection after ischemia/reperfusion by coupling mitochondrial functional preservation with mitophagy reactivation. - Source: PubMed
Publication date: 2026/08/05
Li DingyangZhu FukaiFan ZhongxiongYu ShujieLiao YuanKou LeleZheng RuifangLi Zhijian - The liver receives microbe and host signals from the intestine via the portal vein, thereby connecting the gut to systemic physiology. Homeostatic control of the timing of systemic responses is critical to prevent the expansion and dissemination of gut microbes and to mitigate untoward effects from prolonged systemic inflammation, however these mechanisms remain enigmatic. Here, to determine the role of the liver in coordinating systemic immune responses to enteric infection, matched measurements of global gene expression profiles were collected from the murine liver and intestinal epithelium throughout the course of enteric infection and clearance of Citrobacter rodentium, a mouse model of infectious colitis. These data revealed metabolic suppression in the liver during the peak of infection and a long-lived immune signaling pattern in the colon associated with CD4 and CD8 T cell infiltration that persisted beyond the clearance of infection. Furthermore, an early inflammatory signal was detected in the liver that resolved before the peak of disease and pathogen colonization. This self-limited, early signal depended on the pathogen's virulence program and correlated with the timing of a corresponding systemic response, including circulating TNF-α and IL-6, key mediators of acute-phase proteins. These results uncover the temporal pattern of hepatic changes in response to the course of intestinal infection and provide correlative evidence that an early pulse of gene expression in the liver coordinates and limits the duration of the systemic acute-phase protein response. - Source: PubMed
Publication date: 2026/08/05
Hasegawa YukoOsaki AkinaSuzuki MasatakaYan TingCampbell Ian WWaldor Matthew K - The present study investigated the protective effects of ferulic acid against behavioral and neurochemical alterations induced by early life stress (ELS) using a maternal separation model in mice. Swiss albino mouse pups were subjected to maternal separation from postnatal day 2 to 14. During adulthood, animals received ferulic acid (40 and 80 mg/kg, p.o.) or fluoxetine (20 mg/kg, p.o.) for 15 days. Behavioral assessments included the elevated plus maze, open field test, tail suspension test, and Morris water maze. Oxidative stress, inflammatory, cholinergic, monoaminergic, and neuroendocrine parameters were evaluated in the hippocampus and cerebral cortex. Maternal separation stress produced significant anxiety-like and depressive-like behaviors, impaired spatial learning and memory, elevated corticosterone levels, increased thiobarbituric acid reactive substances (TBARS), nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and acetylcholinesterase (AChE) activity, and decreased reduced glutathione (GSH), serotonin, and dopamine levels in both hippocampal and cortical brain regions. Ferulic acid treatment significantly attenuated behavioral deficits, reduced corticosterone concentrations, restored antioxidant status, suppressed inflammatory mediators, normalized AChE activity, and increased serotonin and dopamine levels. Correlation analysis revealed significant associations between behavioral performance and neurochemical alterations, indicating that improvements in cognitive and affective outcomes were accompanied by normalization of oxidative stress, neuroinflammatory, cholinergic, monoaminergic, and neuroendocrine disturbances. These findings demonstrate that ferulic acid attenuates the long-term behavioral and neurochemical consequences of ELS and support further investigation of its neuroprotective potential in stress-related neurobehavioral disorders. - Source: PubMed
Publication date: 2026/07/21
Simran Singh VarinderKanwar NavjotSingh ManjinderSingh TanveerSingh Thakur GurjeetGrewal Amarjot KaurAhmad Sheikh FAl-Mazroua Haneen A - People with psoriasis are at increased risk for nonmelanoma skin cancers (NMSC) and melanoma. Conventional immunosuppressants and TNF-α inhibitors may further increase skin malignancies, while the risks associated with other biologics are less clear. This study aimed to determine skin malignancy risks in psoriasis patients treated with cyclosporine, methotrexate, TNF-α inhibitors, IL-12/23, IL-17, and IL-23 inhibitors. - Source: PubMed
Woodie Brad RFreking Justin ARivin Gabrielle MFleischer Alan B - Psoriasis is a chronic inflammatory condition affecting approximately 3% of adults in the United States (US). While biologic therapies have transformed treatment for psoriasis, the speed and efficacy of response vary among biologics. This network meta-analysis (NMA) evaluates the efficacy and speed of response of interleukin (IL)-17 and IL-23, and tumor necrosis factor-alpha (TNF-alpha) inhibitors during the first 8 weeks of treating moderate-to-severe plaque psoriasis. - Source: PubMed
Shami M ZaidAmara ShivkarShimon Stephanie VKest IsabellaIslam Rahib KMoffatt LucianoLebwohl Mark