Monkey TNF_alpha ELISPOT kit
- Known as:
- Monkey TNF_alpha ELISPOT reagent
- Catalog number:
- CT133-PB2
- Product Quantity:
- 2-plate
- Category:
- -
- Supplier:
- U-CyTech
- Gene target:
- Monkey TNF_alpha ELISPOT kit
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Related articles to: Monkey TNF_alpha ELISPOT kit
- Stroke-Associated Pneumonia (SAP) is one of the leading causes of sepsis and ICU mortality among stroke patients, attributed to dysregulated immune responses as well as multiple MODES of cell death. Jiajiang Xuming Decoction (JXD) is a traditional Chinese medicine (TCM) formula to treat the symptoms of Wind-Phlegm-Stasis Obstruction Syndrome, blamed for all SAP-related sepsis. - Source: PubMed
Publication date: 2026/07/16
Li ZezhaoWang JieHong ZhenLi MengyaoLiu TianWang YueMen Lianchao - ATP binding cassette (ABC) transporters are active efflux proteins that move substrates against the gradient via hydrolysis of ATP, and regulate fetal metabolic homeostasis and chemical exposure. The maternal-fetal interface represents a barrier for key transporters involved in xenobiotic efflux, reverse cholesterol transport, bile acid handling, metabolism of steroid hormones and immune tolerance. We combine recent data from cryo-electron microscopy-based structure with recent single-cell transcriptomic data and studies of placenta pharmacology to explore the underlying mechanism of transporter dysfunction in preeclampsia, intrahepatic cholestasis of pregnancy, preterm birth, gestational diabetes mellitus, intrauterine growth restriction, and early miscarriage. NRF2-dependent antioxidant signaling, HIF-1α-dependent suppression of BCRP under hypoxia, cytokine-dependent downregulation by TNF-α and IL-1β, and autophagy. Key translation opportunities in clinical pharmacogenomics are highlighted, such as near-term ABCG2 Q141K genotyping for glyburide prescribing in gestational diabetes, and ABCB4 variant profiling for cholestasis risk. - Source: PubMed
Publication date: 2026/07/16
Wang Xian-HongSaeed GhazalaAfzal AliSaddozai Umair Ali KhanShao Gui-MinRehman AmnaHamid Syeda EishaPan Si-YingJi Xin-YingKhawar Muhammad Babar - The role of saturated fatty acid-induced immunometabolic stress in macrophage dysfunction during metabolic disease remains incompletely understood, particularly the interplay between inflammatory signaling and intracellular lipid handling. We employed a tightly controlled palmitic acid (PA)-based lipotoxicity model in PMA-differentiated U937-derived human macrophage-like cells to investigate how lipid excess reshapes inflammatory responses and to evaluate the modulatory effects of cannabidiol (CBD). PA exposure induced a metabolically stressed yet viable macrophage phenotype, characterized by a broad cytokine remodeling profile. This included induction of classical proinflammatory cytokines such as interleukin (IL)-6, together with activation of inflammasome-associated cytokines IL-1β and IL-18 and additional immunoregulatory mediators, while tumor necrosis factor alpha (TNF-α) contributed to the overall inflammatory profile in a multivariate analysis. These changes were accompanied by a significant, time-dependent storage of intracellular triglycerides (TG) consistent with lipid overload and altered lipid handling. CBD co-treatment did not compromise cell viability but selectively attenuated PA-induced inflammatory response in a cytokine-dependent manner, with the most significant reduction observed at higher concentrations. In parallel, CBD significantly reduced intracellular TG accumulation under lipotoxic conditions. Collectively, these findings define a lipotoxicity-associated macrophage phenotype driven by saturated fatty acids and identify CBD as a context-dependent modulator of immunometabolic inflammation. This work provides a controlled experimental framework to study lipid-driven inflammatory dysfunction and supports the potential of CBD as a targeted strategy to modulate metabolic inflammation without broadly suppressing immune function. - Source: PubMed
Publication date: 2026/07/16
Rueda-Munguía MayteRodriguez-Moncayo RobertoLuévano-Martínez Luis AlbertoGarcía-Rivas GerardoCastillo Elena CristinaLozano Omar - This study investigated whether a fucosterol-standardized extract (SFE) attenuates muscle atrophy by regulating inflammatory responses and muscle protein turnover in vitro and in vivo. In tumor necrosis factor-α-stimulated C2C12 myotubes, SFE suppressed inflammatory cytokine expression ( and ) and attenuated protein degradation by downregulating muscle-specific ubiquitin ligases ( and ) via restored forkhead box O3a phosphorylation. SFE also restored myogenic regulatory factors ( and ) and reactivated the phosphoinositide 3-kinase/protein kinase B/mechanistic target of rapamycin (PI3K/Akt/mTOR) signaling pathway, indicating recovery of anabolic signaling. In immobilization-induced muscle atrophy mice, SFE improved grip strength and preserved skeletal muscle mass, accompanied by an increase in muscle fiber cross-sectional area. At the molecular level, SFE mitigated inflammatory responses and restored imbalance between protein synthesis and degradation in the tibialis anterior muscle. Collectively, these findings demonstrate that SFE attenuates immobilization-induced muscle atrophy by suppressing inflammation and restoring PI3K/Akt/mTOR-mediated muscle protein homeostasis. - Source: PubMed
Publication date: 2026/05/29
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Publication date: 2026/07/29
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