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genlisa mouse interleukin 10 (il-10 / il10) elisa  (Krishgen Biosystems)


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    Krishgen Biosystems genlisa mouse interleukin 10 (il-10 / il10) elisa
    Genlisa Mouse Interleukin 10 (Il 10 / Il10) Elisa, supplied by Krishgen Biosystems, used in various techniques. Bioz Stars score: 94/100, based on 29 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/il+10/GENLISA+Mouse+Interleukin+10+(IL-10+%2F+IL10)+ELISA/custom%40kb2072%4010%2E1186%2Fs41110-026-00524-w
    Average 94 stars, based on 29 article reviews
    genlisa mouse interleukin 10 (il-10 / il10) elisa - by Bioz Stars, 2026-10
    94/100 stars

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    Related Articles

    Enzyme-linked Immunosorbent Assay:

    Article Title: Sulforaphane-Mediated Multitarget Therapeutic Effects in Methylmercury-Induced ALS-Like Pathology: Comparative Analysis and Multifaceted Approach to Neuroprotection and Systemic Recovery.
    Article Snippet: Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disorder marked by motor neuron loss driven by oxidative stress, neuroinflammation, and dysregulated survival signaling.. The objective of this study was to evaluate the neuroprotective efficacy and safety of sulforaphane (SUFP) in a methylmercury (MMHg+)-induced preclinical rat model of ALS, with comparison to omaveloxolone (OVX) and dimethyl fumarate (DIMT).. SUFP treatment, particularly at 4 mg/kg, significantly restored antioxidant defense mechanisms through upregulation of Nrf2, HO-1, and SIRT1 while suppressing proinflammatory cytokines (IL-1β, TNF-α), apoptotic markers (Bax, caspase-3), and stress-related signaling pathways including p75NTR, PI3K/Akt, and MAPKs.

    Article Title: Ranolazine neuroprotection against middle cerebral artery occlusion/reperfusion ischemic injury via modulation of brain-derived neurotrophic factor and brain mitochondrial tu translation elongation factor (TUFM).
    Article Snippet: Cerebral ischemia is one of the leading contributors to mortality and morbidity worldwide (Zhu et al. 2022), caused by the obstruction of cerebral blood vessels due to blood clots or emboli.. This culminates in insufficient oxygen and nutrient delivery, thereby inducing cellular death and tissue injury within the affected cerebral area (Yu et al. 2022).. The primary therapeutic approaches for ischemic stroke include thrombolytic medications, antiplatelet agents, and anticoagulants, which aim to promote increased cerebral blood perfusion (Tsai et al. 2015).

    Article Title: Mechanisms of repetitive LPS exposure-induced toxicity in murine model via Toll-like receptor 4 mediated NF-κB/NLRP3/COX-2 signalling: An in vivo and in silico analysis.
    Article Snippet: Blood-borne lipopolysaccharide (LPS) is a potent trigger of sepsis that can progress to sustained inflammation, immune dysregulation, chronic tissue injury, and multi-organ failure.. We investigated the acute and chronic effects of repeated LPS exposure (up to 5-days) on gut-thyroid axis of mice.. Swiss albino mice/female/8 weeks were maintained in two batches, treated with saline/LPS (1mg/kg bw) intraperitoneally for 5-days, then divided into three groups: Group-I/control (saline), Group-II/LPS5d.

    Article Title: Mitochondrial epigenetic remodeling and integrated stress response induced by Microcystin-LR: Experimental evidence and preliminary PP2A structural targeting.
    Article Snippet: MC-LR, a potent cyanotoxin produced by specific kinds of cyanobacteria, is widely acknowledged for its cytotoxic effects; however, its role in mitochondrial-mediated epigenetic regulation remains poorly characterized.. This study examined the mitochondrial integrated stress response and associated epigenetic changes following exposure to varying concentrations of MC-LR.. Elevated mitochondrial reactive oxygen species (mtROS) indicated disrupted mitochondrial function and dynamics, potentially contributing to reduced cell viability.

    Article Title: Probiotics as an Adjunct Ameliorates Ovarian Toxicity in Endotoxemic Mice via Modulating TLR 4/MyD88/NF-κB Signalling Pathway: Insights from In Vivo and In Silico Study.
    Article Snippet: .. Mouse NTS/NN (KLM2299), NF-κB (KLN1350), IL-10 (KB2072), and estradiol (E2) ELISA kits were purchased from Krishgen Biosystems (Mumbai, India), whereas LH and FSH ELISA kits were from DRG Instruments (Marburg, Germany). .. The rest of the chemicals and reagents were purchased from Himedia (Mumbai, India).

    Article Title: Microglial Dysfunction Mediated by Pb and Amyloid Beta Peptides as a Possible Mechanism of Neurotoxicity.
    Article Snippet: This study delves into the inflammatory and degenerative impacts of lead (Pb) toxicity and amyloid beta peptides (Aβpeptide 1–40 and Aβpeptide 25–35) on brain cells, particularly by fostering M1 polarization in microglial cells and subsequent neuronal cell death, crucial in conditions like Alzheimer's disease.. Microglia were exposed to IC50 concentrations of Pb, and Aβpeptide 1–40 and Aβpeptide 25–35 exhibited notable increases in intracellular ROS levels (32.95%) upon exposure to combinatorial treatments.. Moreover, there was a significant decline in total antioxidant capacity to 69.57%, suggesting oxidative damage and compromised cellular defenses against stress, coupled with heightened glutamate levels (921.3 μM).

    Pyrolysis Gas Chromatography:

    Article Title: Ranolazine neuroprotection against middle cerebral artery occlusion/reperfusion ischemic injury via modulation of brain-derived neurotrophic factor and brain mitochondrial tu translation elongation factor (TUFM).
    Article Snippet: Cerebral ischemia is one of the leading contributors to mortality and morbidity worldwide (Zhu et al. 2022), caused by the obstruction of cerebral blood vessels due to blood clots or emboli.. This culminates in insufficient oxygen and nutrient delivery, thereby inducing cellular death and tissue injury within the affected cerebral area (Yu et al. 2022).. The primary therapeutic approaches for ischemic stroke include thrombolytic medications, antiplatelet agents, and anticoagulants, which aim to promote increased cerebral blood perfusion (Tsai et al. 2015).



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    Mechanical force modulates macrophage <t>M2</t> polarization on PEEK surfaces. (A) The expression levels of mechanical perception (PIEZO1, YAP1) and polarization‐related proteins (iNOS, CD206, STAT6/p‐STAT6, NF‐κB/p‐NF‐κB) in dynamically cultured RAW264.7, determined by Western blot. (B) Gene expression in RAW264.7 were cultured under dynamic and static conditions for 12 h. (C) SEM images of RAW264.7 under static and dynamic culture conditions (scale bar: 10 µm). (D) Confocal fluorescence images of CD206, PIEZO1, iNOS, IL10, YAP1 and ITGB1 in macrophages under dynamic and static conditions (scale bar: 100 µm). The average fluorescence intensity of (E) CD206, IL‐10, (F) PIEZO1, YAP1, and (G) iNOS, ITGB1 were statistically analyzed. Shown are mean values ± SD (n = 3 independent experiments, each with 3 technical replicates), * P < 0.05, ** P < 0.01, and *** P < 0.001, ns, no significant difference. 2‐way ANOVA was used in (B) and (E–G).
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    circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of <t>IL-10,</t> TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.
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    Image Search Results


    Mechanical force modulates macrophage M2 polarization on PEEK surfaces. (A) The expression levels of mechanical perception (PIEZO1, YAP1) and polarization‐related proteins (iNOS, CD206, STAT6/p‐STAT6, NF‐κB/p‐NF‐κB) in dynamically cultured RAW264.7, determined by Western blot. (B) Gene expression in RAW264.7 were cultured under dynamic and static conditions for 12 h. (C) SEM images of RAW264.7 under static and dynamic culture conditions (scale bar: 10 µm). (D) Confocal fluorescence images of CD206, PIEZO1, iNOS, IL10, YAP1 and ITGB1 in macrophages under dynamic and static conditions (scale bar: 100 µm). The average fluorescence intensity of (E) CD206, IL‐10, (F) PIEZO1, YAP1, and (G) iNOS, ITGB1 were statistically analyzed. Shown are mean values ± SD (n = 3 independent experiments, each with 3 technical replicates), * P < 0.05, ** P < 0.01, and *** P < 0.001, ns, no significant difference. 2‐way ANOVA was used in (B) and (E–G).

    Journal: Advanced Science

    Article Title: Alternating Shear Force of Respiration Regulates Cell Interactions of Fibroblasts and Macrophages to Promote Soft Tissue Integration of Chest Wall Polyetheretherketone Implants

    doi: 10.1002/advs.77118

    Figure Lengend Snippet: Mechanical force modulates macrophage M2 polarization on PEEK surfaces. (A) The expression levels of mechanical perception (PIEZO1, YAP1) and polarization‐related proteins (iNOS, CD206, STAT6/p‐STAT6, NF‐κB/p‐NF‐κB) in dynamically cultured RAW264.7, determined by Western blot. (B) Gene expression in RAW264.7 were cultured under dynamic and static conditions for 12 h. (C) SEM images of RAW264.7 under static and dynamic culture conditions (scale bar: 10 µm). (D) Confocal fluorescence images of CD206, PIEZO1, iNOS, IL10, YAP1 and ITGB1 in macrophages under dynamic and static conditions (scale bar: 100 µm). The average fluorescence intensity of (E) CD206, IL‐10, (F) PIEZO1, YAP1, and (G) iNOS, ITGB1 were statistically analyzed. Shown are mean values ± SD (n = 3 independent experiments, each with 3 technical replicates), * P < 0.05, ** P < 0.01, and *** P < 0.001, ns, no significant difference. 2‐way ANOVA was used in (B) and (E–G).

    Article Snippet: To induce M2 phenotype, M0 macrophages were stimulated with 10 ng/mL IL‐10 (HY‐P70517, MedChemExpress LLC., USA) and 20 ng/mL IL‐4 (HY‐ P70653 , MedChemExpress LLC., USA)

    Techniques: Expressing, Cell Culture, Western Blot, Gene Expression, Fluorescence

    circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

    Journal: Non-coding RNA Research

    Article Title: CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma

    doi: 10.1016/j.ncrna.2026.03.003

    Figure Lengend Snippet: circSMAD4 drives tumor-educated M2-like polarization of macrophages and promotes tumor-cell aggressiveness. (A) Workflow for generating TC-hMDMs and TC-BMDMs, circSMAD4 knockdown, and downstream functional assays. (B) RT–qPCR analysis of M1-associated markers (MHC-II [HLA-DRA in TC-hMDMs; H2-Ab1 in TC-BMDMs], NOS2, and CD86) and M2-associated markers (CD163, CD206, and ARG1) in TC-hMDMs and TC-BMDMs. (C) Representative flow-cytometry histograms for HLA-DR, iNOS, CD86, CD163, CD206, and ARG1 in TC-hMDMs. Gating strategy and marker thresholds were defined based on FMO controls (see ). (D) Flow-cytometry quantification of marker-positive cells in TC-hMDMs and TC-BMDMs. (E) ELISA of IL-10, TGF-β, and iNOS in culture supernatants. (F) CCK-8 assays of A549 and LLC cells. (G) Colony-formation assays of A549 and LLC cells with quantification. (H) Bioluminescence-based growth readouts of patient-derived LUAD organoids (PDO #1 and PDO #2) after co-culture with TC-hMDMs. (I) Immunoblot analysis of EMT-related proteins (E-cadherin, N-cadherin, Vimentin) in A549 and LLC cells. (J) Transwell migration and invasion assays of A549 and LLC cells with quantification. Scale bar, 50 μm. ∗P < 0.05; ∗∗P < 0.01; ∗∗∗P < 0.001; ∗∗∗∗P < 0.0001; ns, not significant.

    Article Snippet: For mouse experiments, mouse IL-10 was measured using the Mouse IL-10 ELISA Kit (R&D Systems, Cat# M1000B), and mouse TGF-β1 was measured using the Mouse TGF beta-1 ELISA Kit (Invitrogen, Cat# BMS608-4), following the manufacturers’ instructions.

    Techniques: Knockdown, Functional Assay, Quantitative RT-PCR, Flow Cytometry, Marker, Enzyme-linked Immunosorbent Assay, CCK-8 Assay, Derivative Assay, Co-Culture Assay, Western Blot, Migration