ARGI1_MOUSE Arg1 ELISA tesk kit
- Known as:
- ARGI1_MOUSE Arg1 Enzyme-linked immunosorbent assay test tesk reagent
- Catalog number:
- gen15017
- Product Quantity:
- 1
- Category:
- Peptides
- Supplier:
- Other suppliers
- Gene target:
- ARGI1_MOUSE Arg1 ELISA tesk kit
Related genes to: ARGI1_MOUSE Arg1 ELISA tesk kit
- Gene:
- ARG1 NIH gene
- Name:
- arginase 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 6q23.2
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: ARGI1_MOUSE Arg1 ELISA tesk kit
Related articles to: ARGI1_MOUSE Arg1 ELISA tesk kit
- Anastomotic leakage continues to be a severe and prevalent complication in colorectal surgery, leading to elevated morbidity and mortality rates despite modern advancements in surgical and perioperative care. To address this persistent clinical challenge, the aim of the present study was to engineer a biocompatible poly(lactic-co-glycolic acid) (PLGA) matrix designed for the sustained release of melatonin, subsequently evaluating its therapeutic efficacy in promoting colon anastomotic repair. Seventy-two male Wistar albino rats were randomly assigned to three experimental groups: anastomosis (n = 24); anastomosis + matrix (n = 24); and anastomosis + melatonin-loaded matrix (n = 24). Anastomotic segments were harvested on postoperative days 3 and 7, and colonic bursting pressure was measured as a functional indicator of anastomotic integrity. The melatonin-loaded matrix significantly enhanced anastomotic healing on postoperative day 7. Melatonin delivery: (1) markedly reduced the gene expression of pro-inflammatory cytokines; (2) modulated iNOS, COX-2 and MPO expression on both days 3 and 7; (3) decreased HO-1 and catalase expression on day 7; (4) promoted collagen synthesis; (5) enhanced collagen deposition through upregulation of Arg-1; and (6) regulated ADAM10 and ADAM17 gene expression. These results are correlated with the histological analysis findings. Collectively, controlled release of melatonin via a PLGA-based biomaterial matrix promotes colon anastomosis healing. This strategy represents a promising translational approach for reducing postoperative anastomotic complications. - Source: PubMed
Publication date: 2026/09/27
Demir UfukYurtgezen Zekiye GülfemErbil GülfemGökçe Oruç NumanOral AyhanUzun Metehan - The M1-to-M2 macrophage phenotypic switch is critical for resolving inflammation and restoring homeostasis in hypoxic lung injury, but the underlying molecular mechanisms are unclear. Here, we show that hypoxia-induced histone lactylation (Kla) upregulates FTO via HIF1a-P300 interaction; lactylation-driven FTO then promotes late-stage M2 polarization by stabilizing Arg1 mRNA through the mA-YTHDF2 axis. Mechanistically, HIF1a/YY1 liquid-liquid phase separation (LLPS) regulates macrophage glycolysis and oxidative phosphorylation (OXPHOS) via the cGAS-STING pathway downstream of lactylation. Importantly, lactylation exerts context-dependent dual effects: physiological lactylation in wild-type mice facilitates M2 polarization, maintains metabolic balance, and promotes lung repair, whereas excessive lactylation in IL-10-deficient mice disrupts the FTO-Arg1 cascade, perturbs metabolism, blocks M2 polarization, and aggravates injury. Collectively, histone lactylation is a core switch governing macrophage polarization and metabolic homeostasis in hypoxic lung injury, with its function dictated by IL-10 status and lactylation abundance. - Source: PubMed
Publication date: 2026/09/25
Zhao XingwangZhang MengjieYin JunLiao JingyiLi DenghuiTian ZhiqiangYou YiZhang LonglongNi Bing - The study was conducted to investigate effects of dietary antimicrobial peptide, tilapia-derived endogenous piscidin 4 (TP4), on growth performance, antioxidant capacity, immune response and disease resistance of juvenile Nile Tilapia (). - Source: PubMed
Publication date: 2026/09/11
Zhang WencongWang LeiZhao JinliangYun BiaoQian Xueqiao - subsp. (SEZ) causes severe infections, but the role of the negative regulator interleukin-1 receptor-associated kinase M (IRAK-M) in SEZ-induced inflammation is unclear. In this study, male C57BL/6 mice received a single intraperitoneal injection of SEZ at 2 × 10 CFU and were examined 24 h post-injection. SEZ infection triggered overt jejunal hemorrhage and upregulation of IL-1β, IL-6, and TNF-α mRNA, confirming local inflammation, with a concurrent marked reduction in both mRNA and protein levels of IRAK M in the jejunum, hinting at its possible role. We next used IRAK-M knockout (IRAK-M) mice and found that, compared with the WT+SEZ group, the knockout group displayed more severe jejunal hemorrhage, histopathological scores, and neutrophil infiltration, along with a higher bacterial burden and further elevated pro-inflammatory cytokines and reduced anti-inflammatory cytokine expression. Mechanistically, IRAK-M deficiency in the jejunum further increased the mRNA expression of MyD88, TRIF, TRAF6, IKKα+β, NF-κBp50, and NF-κBp65 and decreased IκBα mRNA compared with the WT+SEZ group. These findings were paralleled at the protein level, as demonstrated by Western blotting for MyD88, TRAF6, and IKKα+β, and by immunofluorescence in peritoneal macrophages. Importantly, IRAK-M deficiency drove a shift toward the M1 macrophage phenotype in both jejunal tissues and peritoneal macrophages, characterized by upregulation of CD16, CD32, CD80, CD86, iNOS, and MHC II, and downregulation of the M2-associated markers Arg1 and CD206. These findings reveal that SEZ infection causes jejunal inflammation and that IRAK-M knockout worsens this condition, pointing to a role for IRAK-M in regulating inflammatory readouts in this model. - Source: PubMed
Publication date: 2026/09/16
Che YuxinXie YiQiu XinyiLin JunxiXiu YixinYu TaoyuZhan XiaoshuLiao JiedanHuang YunfeiYe YaqiongDeng Ziteng - Maternal immune activation (MIA) during pregnancy is a recognized risk factor for neurodevelopmental and neurodegenerative disorders, including Alzheimer's disease. Although the long-term consequences of prenatal inflammation have been extensively investigated, the influence of biological sex on age-related behavioral and hippocampal alterations remains insufficiently understood. MIA was induced in pregnant Wistar rats by the intraperitoneal administration of lipopolysaccharide (100 μg/kg) on gestational day 17. Male and female offspring were examined at 12 months of age. Behavioral patterns were assessed using the Morris water maze and elevated plus maze. Hippocampal neuronal morphology and microglial and astrocytic phenotypes were evaluated by histology and IHC, while the expression of genes associated with inflammation, neurodegeneration, neuroplasticity, oxidative stress, and neurogenesis was determined by RT-qPCR. Prenatal LPS exposure produced persistent behavioral alterations in both sexes but with distinct phenotypes. Both male and female offspring exhibited increased anxiety-like behavior, whereas females showed reduced exploratory activity during spatial memory testing. Female offspring demonstrated more pronounced hippocampal pathology, including an increased relative number of pyknotic hyperchromic neurons, a reduced ramified-to-amoeboid microglia ratio, decreased , and selective upregulation of and , potentially indicating enhanced susceptibility to neurodegenerative processes. In contrast, males maintained predominantly ramified microglia morphology and showed increased expression of the neuronal progenitor gene , possibly suggesting the activation of compensatory mechanisms. Both sexes exhibited hippocampal upregulation of , , , , and , consistent with chronic pro-inflammatory background accompanied by adaptive antioxidant and anti-inflammatory responses. Prenatal immune activation induces long-lasting behavioral, morphological, and molecular alterations that persist into middle age and exhibit marked sexual dimorphism. Female offspring appear more vulnerable to pro-neurodegenerative changes, whereas male offspring activate compensatory neuroprotective pathways that might partially preserve hippocampal function despite sustained pro-inflammatory reactions. These findings highlight sex as a critical biological variable in the long-term consequences of prenatal inflammation and may facilitate the identification of early biomarkers and therapeutic targets for MIA-associated neuropsychiatric and neurodegenerative disorders. - Source: PubMed
Publication date: 2026/09/15
Sentyabreva Alexandra VLyamtsev Alexander SMelnikova Ekaterina AAliper Gleb MKosyreva Anna M