Rat TNF_alpha 50 ug
- Known as:
- Rat TNF_alpha 50 ug
- Catalog number:
- 1052-50
- Product Quantity:
- 50 ug
- Category:
- -
- Supplier:
- Biovis
- Gene target:
- Rat TNF_alpha 50
Related products to: Rat TNF_alpha 50 ug
Related articles to: Rat TNF_alpha 50 ug
- Acute kidney injury (AKI) is associated with dysregulated cysteine (Cys) levels and oxidative stress. Hydrogen sulfide (HS) plays a regulatory role in renal diseases with antioxidant and anti-inflammatory effects. However, tools for real-time monitoring of gas release and therapeutic response remain limited. Herein, we report a cysteine-triggered near-infrared (NIR) fluorescent HS donor platform NIR-NRS (R = Me/Ph/H) based on hemicyanine fluorophores and a thiocarbamate moiety. Notably, NIR-NHS enables efficient HS release accompanied by significant fluorescence enhancement (10-fold), allowing real-time visualization of gas generation. To improve biocompatibility and renal targeting, NIR-NHS was conjugated with bovine serum albumin (BSA) to construct nanoprodrugs (NIR-NHS@BSA and NIR-NHS@BSA). Among them, NIR-NHS@BSA exhibits size-dependent HS release behavior, efficient reactive oxygen species (ROS) scavenging, and oxidative stress recovery. studies demonstrate that NIR-NHS@BSA achieves efficient kidney targeting and allows real-time visualization of HS release in response to elevated Cys levels. In cisplatin-induced AKI models, this system enables imaging-guided evaluation of therapeutic efficacy, reducing inflammatory cytokines (TNF-α and IL-1β). This work establishes an NIR imaging-based analytical platform for real-time monitoring and evaluation of HS-based therapeutics in kidney injury. - Source: PubMed
Publication date: 2026/05/27
Zhu YanyanHe ZiyuDu TianyouZhu BingjianWang Hai-YanYu HuiLiu Yi - Sepsis is a clinical issue with a major impact on in-hospital patients, resulting in multiple organ damage and increased risk of death. Acute kidney injury (AKI) is the most common organ that is vulnerable to sepsis and may progress to renal failure if not treated. Bevacizumab is a biopharmaceutical agent that disrupts the angiogenesis signalling pathway by binding to vascular endothelial growth factor (VEGF) and preventing it from coupling with cognate receptors. The present study aimed to assess the renoprotective potential of bevacizumab against sepsis-induced renal injury. - Source: PubMed
Publication date: 2026/05/27
Qassam HeiderGaen Karrar KareemAzzam AmmarAl-Mudhafar Ahmed MhAlmudhafar Rihab HameedHadi Najah R - Chronic consumption of omega-6-enriched dietary fat may disturb brain redox balance and neuroinflammatory homeostasis. Among the sirtuins, sirtuin 1 (SIRT1) exerts critical neuroprotective functions by suppressing oxidative stress and inflammatory signaling; however, the impact of sunflower oil-based high-fat diets (SO-HFD) on brain SIRT1 activity has not been investigated. - Source: PubMed
Publication date: 2026/05/27
Çavuşoğlu NurayŞekerler TurgutDoğan ÖzgeŞener Azize - During alcoholic liver disease (ALD), alcohol induces functional impairment of LSECs, thereby exacerbating inflammation and fibrosis. This research aims to investigate whether P38γ drives aerobic glycolysis in LSECs via the PFKFB3 signaling axis, thereby participating in the progression of ALD. - Source: PubMed
Publication date: 2026/05/27
Zhang QianYang MiaoZhang YunHu Jing - In this study, we systematically investigated the role of miR-16-2-3p, a microRNA passenger strand derived from the MIR16-2 hairpin, in glucocorticoid resistance (GCR) and its underlying regulatory mechanisms. The results showed that miR-16-2-3p expression was significantly downregulated in patients with GCR and in glucocorticoid-resistant-like inflammatory models, and was positively correlated with glucocorticoid receptor (GR) expression, accompanied by a reduced responsiveness to the glucocorticoid dexamethasone (Dex). Functional experiments demonstrated that overexpression of miR-16-2-3p enhanced the inhibitory effects of Dex on inflammatory cytokines (interleukin [IL]-1β, IL-6, IL-8, and tumour necrosis factor alpha [TNF-α]) and promoted nuclear translocation of the GR, whereas inhibition of miR-16-2-3p expression attenuated the anti-inflammatory effects of Dex. Mechanistically, cAMP response element-binding protein 1 (CREB1) was identified as a direct target of miR-16-2-3p, and CREB1 silencing promoted GR nuclear translocation and enhanced the anti-inflammatory efficacy of Dex. In addition, miR-16-2-3p further suppressed nuclear factor kappa-B (NF-κB) signalling by targeting NF-κB1 (p105), thereby synergistically strengthening the inhibitory effect of Dex on NF-κB. In vivo, overexpression of miR-16-2-3p significantly improved the pathological phenotype of dextran sulphate sodium (DSS)-induced ulcerative colitis (UC) in mice and enhanced the therapeutic effect of Dex. Our findings revealed a dual molecular mechanism by which miR-16-2-3p enhances glucocorticoid sensitivity (GCS) through targeting CREB1 and NF-κB1, providing experimental evidence for its potential as a novel therapeutic agent for GCR. - Source: PubMed
Publication date: 2026/05/27
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