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one step tunel apoptosis assay kit  (Beyotime)


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    Structured Review

    Beyotime one step tunel apoptosis assay kit
    DON reverses PASMC proliferation and <t>apoptosis</t> resistance in MCT-induced PAH rats. Immunohistochemical staining for Ki67 and <t>TUNEL</t> in lung tissue to show the effect of DON on PASMC proliferation and apoptosis in MCT-induced rats in vivo (×400 magnification). Relative positive cells of the pulmonary artery were counted. To further test PASMC proliferative ability in vitro , PASMCs in the Ctrl, MCT, DON groups were isolated and cultured. The proliferative and apoptotic abilities of PASMCs were, respectively, assayed by immunofluorescence staining with EdU and TUNEL. The ratio of EdU and TUNEL positive cells to total cell numbers per high power field (×200 magnification) were calculated. (A) Representative immunohistochemical staining for Ki67 and TUNEL of pulmonary artery samples. (B) Quantitative analysis of Ki67 positive rate. (C) Quantitative analysis of TUNEL positive rate. (D) Statistical analysis of the EdU+ cell rate. (E) Statistical analysis of the apoptosis rate of PASMCs. (F) Representative immunofluorescent staining for EdU of PASMCs. (G) Representative immunofluorescent staining for TUNEL of PASMCs. Ctrl, control; DON, donepezil; DAPI, 4',6-diamidino-2-phenylindole; EdU, 5-ethynyl-20-deoxyuridine; MCT, monocrotaline; OD, optical density; PASMCs, pulmonary artery smooth muscle cells; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling. * P < 0.05, vs. Ctrl group, # P < 0.05, vs. MCT group ( n = 5).
    One Step Tunel Apoptosis Assay Kit, supplied by Beyotime, used in various techniques. Bioz Stars score: 98/100, based on 4093 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/computer+adaptive+testing+(cat)-based+software/One+Step+TUNEL+Apoptosis+Assay+Kit/pmc08005547-96-0-9
    Average 98 stars, based on 4093 article reviews
    one step tunel apoptosis assay kit - by Bioz Stars, 2026-11
    98/100 stars

    Images

    1) Product Images from "Donepezil Ameliorates Pulmonary Arterial Hypertension by Inhibiting M2-Macrophage Activation"

    Article Title: Donepezil Ameliorates Pulmonary Arterial Hypertension by Inhibiting M2-Macrophage Activation

    Journal: Frontiers in Cardiovascular Medicine

    doi: 10.3389/fcvm.2021.639541

    DON reverses PASMC proliferation and apoptosis resistance in MCT-induced PAH rats. Immunohistochemical staining for Ki67 and TUNEL in lung tissue to show the effect of DON on PASMC proliferation and apoptosis in MCT-induced rats in vivo (×400 magnification). Relative positive cells of the pulmonary artery were counted. To further test PASMC proliferative ability in vitro , PASMCs in the Ctrl, MCT, DON groups were isolated and cultured. The proliferative and apoptotic abilities of PASMCs were, respectively, assayed by immunofluorescence staining with EdU and TUNEL. The ratio of EdU and TUNEL positive cells to total cell numbers per high power field (×200 magnification) were calculated. (A) Representative immunohistochemical staining for Ki67 and TUNEL of pulmonary artery samples. (B) Quantitative analysis of Ki67 positive rate. (C) Quantitative analysis of TUNEL positive rate. (D) Statistical analysis of the EdU+ cell rate. (E) Statistical analysis of the apoptosis rate of PASMCs. (F) Representative immunofluorescent staining for EdU of PASMCs. (G) Representative immunofluorescent staining for TUNEL of PASMCs. Ctrl, control; DON, donepezil; DAPI, 4',6-diamidino-2-phenylindole; EdU, 5-ethynyl-20-deoxyuridine; MCT, monocrotaline; OD, optical density; PASMCs, pulmonary artery smooth muscle cells; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling. * P < 0.05, vs. Ctrl group, # P < 0.05, vs. MCT group ( n = 5).
    Figure Legend Snippet: DON reverses PASMC proliferation and apoptosis resistance in MCT-induced PAH rats. Immunohistochemical staining for Ki67 and TUNEL in lung tissue to show the effect of DON on PASMC proliferation and apoptosis in MCT-induced rats in vivo (×400 magnification). Relative positive cells of the pulmonary artery were counted. To further test PASMC proliferative ability in vitro , PASMCs in the Ctrl, MCT, DON groups were isolated and cultured. The proliferative and apoptotic abilities of PASMCs were, respectively, assayed by immunofluorescence staining with EdU and TUNEL. The ratio of EdU and TUNEL positive cells to total cell numbers per high power field (×200 magnification) were calculated. (A) Representative immunohistochemical staining for Ki67 and TUNEL of pulmonary artery samples. (B) Quantitative analysis of Ki67 positive rate. (C) Quantitative analysis of TUNEL positive rate. (D) Statistical analysis of the EdU+ cell rate. (E) Statistical analysis of the apoptosis rate of PASMCs. (F) Representative immunofluorescent staining for EdU of PASMCs. (G) Representative immunofluorescent staining for TUNEL of PASMCs. Ctrl, control; DON, donepezil; DAPI, 4',6-diamidino-2-phenylindole; EdU, 5-ethynyl-20-deoxyuridine; MCT, monocrotaline; OD, optical density; PASMCs, pulmonary artery smooth muscle cells; TUNEL, terminal deoxynucleotidyl transferase dUTP nick end labeling. * P < 0.05, vs. Ctrl group, # P < 0.05, vs. MCT group ( n = 5).

    Techniques Used: Immunohistochemical staining, Staining, TUNEL Assay, In Vivo, In Vitro, Isolation, Cell Culture, Immunofluorescence, Control

    M2-macrophages inhibited PASMC proliferation and promoted its apoptosis. PASMCs in MCT-induced rats were isolated and cultured, which were co-cultured with the supernatant of BMDMs isolated from the Ctrl, MCT and DON group, respectively. After 24 h cultivation, the proliferative and apoptotic abilities of PASMCs were, respectively, assayed by EdU and TUNEL Assay Kit. The ratio of EdU and TUNEL positive cells to total cell numbers per high power field (×200 magnification) were calculated. (A) EdU stain to test proliferation of PASMCs. (B) Statistical analysis of EdU+ cell rate. (C) TUNEL assay to detect apoptosis of PASMCs. (D) Statistical analysis of apoptosis rate. BMDMs, bone marrow-derived macrophages; Ctrl, control; DON, donepezil; DAPI, 4',6-diamidino-2-phenylindole; EdU, 5-ethynyl-20-deoxyuridine; MCT, monocrotaline; PASMCs, pulmonary artery smooth muscle cells; TUNEL, Terminal deoxynucleotidyl transferase dUTP nick end labeling. * P < 0.05, vs. Ctrl group, # P < 0.05, vs. MCT group ( n = 5).
    Figure Legend Snippet: M2-macrophages inhibited PASMC proliferation and promoted its apoptosis. PASMCs in MCT-induced rats were isolated and cultured, which were co-cultured with the supernatant of BMDMs isolated from the Ctrl, MCT and DON group, respectively. After 24 h cultivation, the proliferative and apoptotic abilities of PASMCs were, respectively, assayed by EdU and TUNEL Assay Kit. The ratio of EdU and TUNEL positive cells to total cell numbers per high power field (×200 magnification) were calculated. (A) EdU stain to test proliferation of PASMCs. (B) Statistical analysis of EdU+ cell rate. (C) TUNEL assay to detect apoptosis of PASMCs. (D) Statistical analysis of apoptosis rate. BMDMs, bone marrow-derived macrophages; Ctrl, control; DON, donepezil; DAPI, 4',6-diamidino-2-phenylindole; EdU, 5-ethynyl-20-deoxyuridine; MCT, monocrotaline; PASMCs, pulmonary artery smooth muscle cells; TUNEL, Terminal deoxynucleotidyl transferase dUTP nick end labeling. * P < 0.05, vs. Ctrl group, # P < 0.05, vs. MCT group ( n = 5).

    Techniques Used: Isolation, Cell Culture, TUNEL Assay, Staining, Derivative Assay, Control

    Schematic illustration of the effect of DON on ameliorating MCT-induced PAH by regulating M2 macrophage activation. In the MCT-induced PAH rat model, parasympathetic activity is reduced, inflammatory response and M2-macrophages are activated, and the expression of pro-inflammatory factors and pro-proliferation factor Fizz1 is increased, and subsequently increase PASMC proliferation and apoptosis resistance. However, DON enhances parasympathetic nerve activity by reducing AchE activity, and suppresses the inflammatory response and M2-macrophage activation, thereby inhibiting PASMC proliferation and promoting its apoptosis to reverse PAH, which is speculated to be related to decreased expression of Fizz1. AchE, acetylcholinesterase; Fizz1, found in inflammatory zone 1; IL-6, interleukin-6; MCT, monocrotaline; PAH, pulmonary arterial hypertension; PASMCs, pulmonary artery smooth muscle cells; TNF-α, tumor necrosis factor-α.
    Figure Legend Snippet: Schematic illustration of the effect of DON on ameliorating MCT-induced PAH by regulating M2 macrophage activation. In the MCT-induced PAH rat model, parasympathetic activity is reduced, inflammatory response and M2-macrophages are activated, and the expression of pro-inflammatory factors and pro-proliferation factor Fizz1 is increased, and subsequently increase PASMC proliferation and apoptosis resistance. However, DON enhances parasympathetic nerve activity by reducing AchE activity, and suppresses the inflammatory response and M2-macrophage activation, thereby inhibiting PASMC proliferation and promoting its apoptosis to reverse PAH, which is speculated to be related to decreased expression of Fizz1. AchE, acetylcholinesterase; Fizz1, found in inflammatory zone 1; IL-6, interleukin-6; MCT, monocrotaline; PAH, pulmonary arterial hypertension; PASMCs, pulmonary artery smooth muscle cells; TNF-α, tumor necrosis factor-α.

    Techniques Used: Activation Assay, Activity Assay, Expressing

    Related Articles

    TUNEL Assay:

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    Apoptosis Assay:

    Article Title: Targeting the Calcium-mtDNA-cGAS-STING Signaling Nexus: A Novel Redox Mechanism for Nimodipine's Neuroprotection in Traumatic Brain Injury.
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    Article Title: The Mechanism of S-adenosylhomocysteine Hydrolase in Regulating Podocyte Apoptosis and Diabetic Nephropathy via Moap1.
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    Staining:

    Article Title: Low-level exposure to trifluoroacetic acid may induce testicular damage in adolescent mice via ribotoxic stress response and NLRC5-PANoptosome-related signaling.
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    Fluorescence:

    Article Title: Low-level exposure to trifluoroacetic acid may induce testicular damage in adolescent mice via ribotoxic stress response and NLRC5-PANoptosome-related signaling.
    Article Snippet: Trifluoroacetic acid (TFA) is considered a perand polyfluoroalkyl substance (PFAS) by the European Chemicals Agency, yet its potential reproductive toxicity remains poorly understood.. Here, we investigated the testicular effects and underlying mechanisms of TFA exposure in adolescent male mice.. Based on environmental and potential dietary exposure levels, available toxicological and risk-assessment information, and the findings of our preliminary experiment, mice were orally administered TFA at 0.0042, 0.042, 0.42, or 4.2 mg/kg/day for 21 days, followed by a 7-day recovery period.

    Article Title: Integrative multi-omics analysis defines a macrophage-associated phospholipid metabolism signature linked to immune remodeling and prognosis in lung adenocarcinoma.
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    Microscopy:

    Article Title: Low-level exposure to trifluoroacetic acid may induce testicular damage in adolescent mice via ribotoxic stress response and NLRC5-PANoptosome-related signaling.
    Article Snippet: Trifluoroacetic acid (TFA) is considered a perand polyfluoroalkyl substance (PFAS) by the European Chemicals Agency, yet its potential reproductive toxicity remains poorly understood.. Here, we investigated the testicular effects and underlying mechanisms of TFA exposure in adolescent male mice.. Based on environmental and potential dietary exposure levels, available toxicological and risk-assessment information, and the findings of our preliminary experiment, mice were orally administered TFA at 0.0042, 0.042, 0.42, or 4.2 mg/kg/day for 21 days, followed by a 7-day recovery period.

    Article Title: Integrative multi-omics analysis defines a macrophage-associated phospholipid metabolism signature linked to immune remodeling and prognosis in lung adenocarcinoma.
    Article Snippet: Cellular DNA synthesis was assessed using the 5-ethynyl-2′-deoxyuridine (EdU) incorporation assay with the BeyoClick EdU Cell Proliferation Kit (Beyotime) according to the manufacturer’s instructions, and nuclei were counterstained with DAPI. .. Apoptosis was evaluated using the One Step TUNEL Apoptosis Assay Kit (Beyotime) and observed under a fluorescence microscope. ..

    Labeling:

    Article Title: The Mechanism of S-adenosylhomocysteine Hydrolase in Regulating Podocyte Apoptosis and Diabetic Nephropathy via Moap1.
    Article Snippet: Elevated levels of S-adenosylhomocysteine (SAH) in patients with diabetes are closely associated with renal dysfunction.. Inhibition of SAH hydrolase (SAHH) increases SAH levels, promotes apoptosis, and exacerbates streptozotocin (STZ)-induced diabetic nephropathy.. However, the precise mechanism by which SAHH inhibition induces podocyte apoptosis remains unclear.

    Article Title: Biomimetic Dichalcogenide-Hybrid Nanozymes With Glutathione Peroxidase-Like Activity for Liver Protection.
    Article Snippet: Glutathione peroxidase (GPX)-mimetic nanozymes are a promising strategy to restore redox homeostasis, but many existing systems rely on metals and remain limited by cytotoxicity, poor selectivity, and susceptibility to catalytic deactivation.. Inspired by the active-site chemistry of native GPX, we designed dichalcogenide-hybrid mesoporous silica nanoparticles (MSNs) as inorganic–organic nanozymes with tunable sulfur and selenium environments.. Structure–activity analysis showed that GPXlike performance is governed by chalcogen composition, chalcogen density, and spatial proximity of S/Se within the framework, which together regulate reversible disulfide/diselenide redox cycling and substrate access.

    H&E Stain:

    Article Title: Paeoniflorin Promotes Mitophagy Against Acute Kidney Injury via PRDX5-Dependent Inhibition of RACK1.
    Article Snippet: Impaired mitophagy is a core driver of acute kidney injury (AKI), yet effective pharmacological strategies to restore this mitochondrial quality control mechanism remain limited.. Paeoniflorin (Pae), a natural monoterpene glycoside, has shown renoprotective potential, but whether and how it regulates mitophagy remain unclear... This study investigated the protective effects of Pae in mice subjected to bilateral renal ischaemia–reperfusion injury (IRI) and in cisplatin-treated TCMK-1 cells, with renal tubular-specific Prdx5 conditional knockout (Prdx5-CKO) mice used to determine the requirement for PRDX5.

    Immunohistochemistry:

    Article Title: Paeoniflorin Promotes Mitophagy Against Acute Kidney Injury via PRDX5-Dependent Inhibition of RACK1.
    Article Snippet: Impaired mitophagy is a core driver of acute kidney injury (AKI), yet effective pharmacological strategies to restore this mitochondrial quality control mechanism remain limited.. Paeoniflorin (Pae), a natural monoterpene glycoside, has shown renoprotective potential, but whether and how it regulates mitophagy remain unclear... This study investigated the protective effects of Pae in mice subjected to bilateral renal ischaemia–reperfusion injury (IRI) and in cisplatin-treated TCMK-1 cells, with renal tubular-specific Prdx5 conditional knockout (Prdx5-CKO) mice used to determine the requirement for PRDX5.

    Transfection:

    Article Title: Paeoniflorin Promotes Mitophagy Against Acute Kidney Injury via PRDX5-Dependent Inhibition of RACK1.
    Article Snippet: Impaired mitophagy is a core driver of acute kidney injury (AKI), yet effective pharmacological strategies to restore this mitochondrial quality control mechanism remain limited.. Paeoniflorin (Pae), a natural monoterpene glycoside, has shown renoprotective potential, but whether and how it regulates mitophagy remain unclear... This study investigated the protective effects of Pae in mice subjected to bilateral renal ischaemia–reperfusion injury (IRI) and in cisplatin-treated TCMK-1 cells, with renal tubular-specific Prdx5 conditional knockout (Prdx5-CKO) mice used to determine the requirement for PRDX5.

    Enzyme-linked Immunosorbent Assay:

    Article Title: Paeoniflorin Promotes Mitophagy Against Acute Kidney Injury via PRDX5-Dependent Inhibition of RACK1.
    Article Snippet: Impaired mitophagy is a core driver of acute kidney injury (AKI), yet effective pharmacological strategies to restore this mitochondrial quality control mechanism remain limited.. Paeoniflorin (Pae), a natural monoterpene glycoside, has shown renoprotective potential, but whether and how it regulates mitophagy remain unclear... This study investigated the protective effects of Pae in mice subjected to bilateral renal ischaemia–reperfusion injury (IRI) and in cisplatin-treated TCMK-1 cells, with renal tubular-specific Prdx5 conditional knockout (Prdx5-CKO) mice used to determine the requirement for PRDX5.

    Over Expression:

    Article Title: Paeoniflorin Promotes Mitophagy Against Acute Kidney Injury via PRDX5-Dependent Inhibition of RACK1.
    Article Snippet: Impaired mitophagy is a core driver of acute kidney injury (AKI), yet effective pharmacological strategies to restore this mitochondrial quality control mechanism remain limited.. Paeoniflorin (Pae), a natural monoterpene glycoside, has shown renoprotective potential, but whether and how it regulates mitophagy remain unclear... This study investigated the protective effects of Pae in mice subjected to bilateral renal ischaemia–reperfusion injury (IRI) and in cisplatin-treated TCMK-1 cells, with renal tubular-specific Prdx5 conditional knockout (Prdx5-CKO) mice used to determine the requirement for PRDX5.

    Plasmid Preparation:

    Article Title: Paeoniflorin Promotes Mitophagy Against Acute Kidney Injury via PRDX5-Dependent Inhibition of RACK1.
    Article Snippet: Impaired mitophagy is a core driver of acute kidney injury (AKI), yet effective pharmacological strategies to restore this mitochondrial quality control mechanism remain limited.. Paeoniflorin (Pae), a natural monoterpene glycoside, has shown renoprotective potential, but whether and how it regulates mitophagy remain unclear... This study investigated the protective effects of Pae in mice subjected to bilateral renal ischaemia–reperfusion injury (IRI) and in cisplatin-treated TCMK-1 cells, with renal tubular-specific Prdx5 conditional knockout (Prdx5-CKO) mice used to determine the requirement for PRDX5.

    Real-time Polymerase Chain Reaction:

    Article Title: Paeoniflorin Promotes Mitophagy Against Acute Kidney Injury via PRDX5-Dependent Inhibition of RACK1.
    Article Snippet: Impaired mitophagy is a core driver of acute kidney injury (AKI), yet effective pharmacological strategies to restore this mitochondrial quality control mechanism remain limited.. Paeoniflorin (Pae), a natural monoterpene glycoside, has shown renoprotective potential, but whether and how it regulates mitophagy remain unclear... This study investigated the protective effects of Pae in mice subjected to bilateral renal ischaemia–reperfusion injury (IRI) and in cisplatin-treated TCMK-1 cells, with renal tubular-specific Prdx5 conditional knockout (Prdx5-CKO) mice used to determine the requirement for PRDX5.

    SYBR Green Assay:

    Article Title: Paeoniflorin Promotes Mitophagy Against Acute Kidney Injury via PRDX5-Dependent Inhibition of RACK1.
    Article Snippet: Impaired mitophagy is a core driver of acute kidney injury (AKI), yet effective pharmacological strategies to restore this mitochondrial quality control mechanism remain limited.. Paeoniflorin (Pae), a natural monoterpene glycoside, has shown renoprotective potential, but whether and how it regulates mitophagy remain unclear... This study investigated the protective effects of Pae in mice subjected to bilateral renal ischaemia–reperfusion injury (IRI) and in cisplatin-treated TCMK-1 cells, with renal tubular-specific Prdx5 conditional knockout (Prdx5-CKO) mice used to determine the requirement for PRDX5.

    Tissue:

    Article Title: Biomimetic Dichalcogenide-Hybrid Nanozymes With Glutathione Peroxidase-Like Activity for Liver Protection.
    Article Snippet: Glutathione peroxidase (GPX)-mimetic nanozymes are a promising strategy to restore redox homeostasis, but many existing systems rely on metals and remain limited by cytotoxicity, poor selectivity, and susceptibility to catalytic deactivation.. Inspired by the active-site chemistry of native GPX, we designed dichalcogenide-hybrid mesoporous silica nanoparticles (MSNs) as inorganic–organic nanozymes with tunable sulfur and selenium environments.. Structure–activity analysis showed that GPXlike performance is governed by chalcogen composition, chalcogen density, and spatial proximity of S/Se within the framework, which together regulate reversible disulfide/diselenide redox cycling and substrate access.



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