Anti_human iNOS rabbit polyclonal
- Known as:
- Anti_human iNOS host: rabbit pab
- Catalog number:
- ASA905-431
- Product Quantity:
- 1 mL
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Anti_human iNOS rabbit polyclonal
Related genes to: Anti_human iNOS rabbit polyclonal
- Gene:
- NOS2 NIH gene
- Name:
- nitric oxide synthase 2
- Previous symbol:
- NOS2A
- Synonyms:
- iNOS, NOS, HEP-NOS
- Chromosome:
- 17q11.2
- Locus Type:
- gene with protein product
- Date approved:
- 1993-06-15
- Date modifiied:
- 2015-12-04
Related products to: Anti_human iNOS rabbit polyclonal
Related articles to: Anti_human iNOS rabbit polyclonal
- L-arginine (ARG) availability is a critical determinant of macrophage antimicrobial capacity, as it fuels nitric oxide production and other immune effector pathways essential for restricting (Mtb), the causative agent of tuberculosis (TB). L-citrulline (CIT), a precursor in the ARG regeneration cycle, can replenish intracellular ARG pools when transport is limited. However, the comparative and combined effects of exogenous ARG and/or CIT on intracellular Mtb control across macrophage lineages and activation states remain insufficiently defined. This study investigated how supplementation with ARG, CIT or their combination influences Mtb survival in human and murine, primary macrophages and cell line, both in naïve and IFNγ-activated states, and evaluated whether these amino acids can enhance the activity of anti-TB drugs, isoniazid (INH) and rifampicin (RIF). Across a 5-day infection course, both ARG and CIT significantly reduced intracellular Mtb loads relative to untreated cells, with high-dose supplementation eliciting earlier and more sustained inhibition. These effects were amplified in IFNγ-stimulated macrophages, accelerating Mtb control and minimizing dose-dependent differences. Combination of ARG plus CIT at intermediate doses produced additive benefits, most notably in murine macrophages where single-agent effects were limited. Co-supplementation with ARG or CIT improved early antimicrobial effects of INH and RIF in all macrophage types, particularly under IFNγ stimulation. Gene expression analyses revealed coordinated metabolic and inflammatory reprogramming. For example, expression was reduced by amino acid supplementation, while expression was increased, and was significantly upregulated by ARG in IFNγ-stimulated cells, and expression was broadly suppressed in these cells. These findings demonstrate that ARG and CIT reshape macrophage antimicrobial response in a complementary manner, augmenting innate and drug-enhanced control of Mtb. The results support metabolic supplementation with ARG and CIT as a promising host-directed therapeutic approach to improve macrophage-mediated restriction of Mtb infection. - Source: PubMed
Publication date: 2026/05/05
Bhargavi GunapatiShreeram SathyavageeswaranPrioult GuenoleeKumar RanjeetSubbian Selvakumar - Hyaluronic acid, as a natural extracellular matrix component, possesses excellent biocompatibility and moisturizing properties, and demonstrates unique advantages in wound repair. - Source: PubMed
Publication date: 2026/05/04
Zheng ChunfangMai WaifungZou LiqiLi LianyingSun Bingwei - To explore the molecular mechanisms underlying cystoid macular edema (CME) through protein-protein interaction (PPI) network analysis, identifying key regulatory proteins, functional modules, and enriched biological pathways relevant to its pathogenesis. - Source: PubMed
Shariati Mehrdad Motamed - Preeclampsia (PE) remains a leading cause of maternal and perinatal mortality worldwide, and the combined use of Shuangjiang Decoction with Labetalol hydrochloride (SJD-Labetalol) has shown promising therapeutic efficacy in clinical settings. However, the underlying molecular mechanisms remain insufficiently understood. This study integrated GEO dataset analysis with network pharmacology and machine learning approaches to elucidate the therapeutic mechanism of SJD-Labetalol. 83 overlapping drug targets were identified, and ten hub genes were highlighted (IL1A, IFNG, BCL2, REN, XDH, NOS3, NOS2, EGFR, MMP3, and CCK). These hub genes were extensively involved in the HIF-1 signaling pathway, fluid shear stress and atherosclerosis, estrogen signaling pathway and calcium signaling pathway. Molecular docking confirmed strong binding affinities between active ingredients (e.g. Rhein, Baicalein, Tanshinone IIA) and these hub proteins. Machine learning-based diagnostic modeling further identified five hub genes (IFNG, MMP3, NOS2, NOS3, REN) as potential biomarkers for PE, achieving an average ROC-AUC of 0.82 in validation cohorts. In summary, this integrative analysis provides a comprehensive molecular basis for the synergistic antihypertensive, anti-inflammatory, and placental protective effects of SJD-Labetalol, offering novel insights for targeted therapeutic strategies in PE management. - Source: PubMed
Publication date: 2026/05/18
Chen LiZhao QingRen YuefangZhu MengyiDing ZhongyingWang TengfeiYang Weihui - Sarcoidosis is a systemic granulomatous disease that often affects the lungs, lymph nodes, and skin. The pathological hallmark of sarcoidosis is the formation of epithelioid, non-necrotizing granulomas, with CD4 T-helper (Th) type 1 (Th1), Th17, and Th17.1 cells scattering throughout the granuloma. The CXCL16-CXCR6 axis plays a crucial role in the development of inflammatory diseases. However, the precise role of CXCR6 CD4 T cells in sarcoidosis pathogenesis and their therapeutic potential remain unclear. In this study, we confirmed the enrichment of CXCR6 CD4 T cells in the lesional tissue of sarcoidosis patients and Propionibacterium acnes-induced sarcoidosis-like model mice. Flow cytometric analysis and single-cell RNA sequencing revealed that CXCR6 CD4 T cells exhibited a Th17/Th17.1 phenotype and displayed pro-inflammatory characteristics. By performing cell-cell communication analysis and validating the findings with flow cytometry and CXCL16-blockade experiments, we demonstrated an active crosstalk between CXCR6 CD4 T cells and CXCL16 macrophages in mice. Furthermore, treating mice with an anti-CXCR6 monoclonal antibody effectively reduced the mRNA levels of pro-inflammatory genes, including Nos2, Cxcl9, Cxcl10, Il17a, Tnf, and Ifng. In addition, anti-CXCR6 treatment reduced the abundance of Th17 and Th17.1 cells, which was associated with inhibition of downstream mTORC1 signaling. Finally, anti-CXCR6 treatment suppressed granuloma formation and attenuated collagen deposition in the lungs. Taken together, our findings highlight CXCR6 as a promising therapeutic target for inhibiting granuloma formation and pulmonary fibrosis in sarcoidosis. - Source: PubMed
Publication date: 2026/05/16
Han YueyinLiu MengyuanXu WenxiuLi ZhenJiang DingyuanGeng JingGao ShuweiLi ShifengXie BingbingZhu LiliZhang HongbingCostabel UlrichDai HuapingWang Chen