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cck 8 cell counting kit  (Beyotime)


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    Structured Review

    Beyotime cck 8 cell counting kit
    Cck 8 Cell Counting Kit, supplied by Beyotime, used in various techniques. Bioz Stars score: 99/100, based on 24280 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cck+8+kit/Cell+Counting+Kit-8/pmc13122825-71-15-20
    Average 99 stars, based on 24280 article reviews
    cck 8 cell counting kit - by Bioz Stars, 2026-11
    99/100 stars

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    Related Articles

    CCK-8 Assay:

    Article Title: Baicalein Synergizes with Docetaxel in TNBC and the Combination Suppresses AKT/GSK3β/β-Catenin Signaling
    Article Snippet: .. The CCK-8 kit was purchased from Beyotime (Cell Counting Kit-8, cat. no. C0038, Shanghai, China). .. The Annexin V-APC/7-AAD apoptosis detection kit was purchased from KeyGEN BioTECH (cat. no. KGA1026, Nanjing, China).

    Article Title: STAT3/MTND4 Mediates Obesity-Related Seminal Vesicle Injury and Impaired Sperm Motility Via Reactive Oxygen Species /Mitochondrial Dysfunction.
    Article Snippet: 1 Center of Reproduction, Women and Children’s Hospital Affiliated to Ningbo University, No. 339 Liuting Street, Haishu District, Ningbo City, Zhejiang Province 315012, China 2 Internal Medicine, Women and Children’s Hospital Affiliated to Ningbo University, No. 339 Liuting Street, Haishu District, Ningbo City, Zhejiang Province 315012, China Abstract Obesity induces male reproductive dysfunction.. Mitochondrial dysfunction ranks among the mechanisms driving functional impairment.. Notably, Mitochondrial NADH dehydrogenase subunit 4 (MTND4) exerts a pivotal role in sustaining the function of the mitochondrial electron transport chain and cellular energy metabolism.

    Article Title: Effect of Microcurrent Stimulation on Cartilage Regeneration in Engineered Chondrocyte Spheroids
    Article Snippet: .. Cell metabolic activity was measured using the CCK-8 kit (Beyotime Biotechnology, Shanghai, China). ..

    Article Title: Yeast β-1,3/1,6 glucan regulates NRF2 to inhibit ferroptosis and ameliorates aspiration pneumonia in aged mice.
    Article Snippet: Background: Aspiration pneumonia (AP) is a common and serious respiratory disease among the elderly, with current treatments limited primarily to antibiotics and supportive care, highlighting a need for targeted therapies.. Yeast β-1,3/1,6glucan (YBG), a natural polysaccharide derived from yeast cell walls, holds immunomodulatory and antioxidant properties.. However, its mechanism in AP remains unclear.

    Article Title: Cellular mechanism of gain-of-function mutation I173M in sheep MC4R gene identified in year-round and seasonal estrus breeds through whole-genome resequencing
    Article Snippet: .. Cell viability was assessed using the CCK-8 kit (Beyotime, Shanghai, China). ..

    Article Title: Sonogenetic Control of Engineered Probiotics for the Treatment of MASH by Modulating the Gut-Liver Axis.
    Article Snippet: .. .9 Cell/Bacterial Viability Assay he viability of various cell lines (IEC, HCT-8, AML-12, HK-2, SF) and IL22-EcN, with or without US irradiation, was assessed sing an Enhanced CCK-8 kit (Beyotime Biotechnology, C0042). ..

    Article Title: Biodegradable electrospun PLLA/HA-ATE composite polypropylene scaffold for hernia repair applications
    Article Snippet: .. The cell viability detection was carried out in accordance with the instructions of the CCK-8 kit (Beyotime, China). ..

    Article Title: Bio-OPMATCH: A multifunctional biomimetic shape-memory scaffold for repairing osteoporotic bone defects by promoting osteogenesis and inhibiting osteoclastogenesis
    Article Snippet: Osteoporotic bone defects, stemming from an imbalance between osteogenesis and osteoclastogenesis, are characterized by reduced bone strength, heightened brittleness, and often irregular morphology, which contribute to delayed repair and pose challenges for mechanical reconstruction.. There is an urgent need for scaffolds that integrate mechanical adaptability, precise filling capability, and the capacity to regulate bone regeneration.. This study introduces Bio-OPMATCH, a composite scaffold designed to integrate mechanical, structural, and functional matching for osteoporotic bone defect repair, with adaptability to irregular defect morphology.

    Activity Assay:

    Article Title: Effect of Microcurrent Stimulation on Cartilage Regeneration in Engineered Chondrocyte Spheroids
    Article Snippet: .. Cell metabolic activity was measured using the CCK-8 kit (Beyotime Biotechnology, Shanghai, China). ..

    Viability Assay:

    Article Title: Sonogenetic Control of Engineered Probiotics for the Treatment of MASH by Modulating the Gut-Liver Axis.
    Article Snippet: .. .9 Cell/Bacterial Viability Assay he viability of various cell lines (IEC, HCT-8, AML-12, HK-2, SF) and IL22-EcN, with or without US irradiation, was assessed sing an Enhanced CCK-8 kit (Beyotime Biotechnology, C0042). ..

    Irradiation:

    Article Title: Sonogenetic Control of Engineered Probiotics for the Treatment of MASH by Modulating the Gut-Liver Axis.
    Article Snippet: .. .9 Cell/Bacterial Viability Assay he viability of various cell lines (IEC, HCT-8, AML-12, HK-2, SF) and IL22-EcN, with or without US irradiation, was assessed sing an Enhanced CCK-8 kit (Beyotime Biotechnology, C0042). ..

    Staining:

    Article Title: Bio-OPMATCH: A multifunctional biomimetic shape-memory scaffold for repairing osteoporotic bone defects by promoting osteogenesis and inhibiting osteoclastogenesis
    Article Snippet: Osteoporotic bone defects, stemming from an imbalance between osteogenesis and osteoclastogenesis, are characterized by reduced bone strength, heightened brittleness, and often irregular morphology, which contribute to delayed repair and pose challenges for mechanical reconstruction.. There is an urgent need for scaffolds that integrate mechanical adaptability, precise filling capability, and the capacity to regulate bone regeneration.. This study introduces Bio-OPMATCH, a composite scaffold designed to integrate mechanical, structural, and functional matching for osteoporotic bone defect repair, with adaptability to irregular defect morphology.



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    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the <t>CCK‐8</t> assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.
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    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the <t>CCK‐8</t> assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.
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    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the <t>CCK‐8</t> assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.
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    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the <t>CCK‐8</t> assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.
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    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the <t>CCK‐8</t> assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.
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    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the <t>CCK‐8</t> assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.
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    Beyotime cck 8 kit
    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the <t>CCK‐8</t> assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.
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    Beyotime cell counting kit 8 cck 8
    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the <t>CCK‐8</t> assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.
    Cell Counting Kit 8 Cck 8, supplied by Beyotime, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Image Search Results


    (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the CCK‐8 assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.

    Journal: CNS Neuroscience & Therapeutics

    Article Title: ATF3 Promotes Solasonine‐Triggered Ferroptosis in Glioma Cells by Suppressing Glycolysis

    doi: 10.1002/cns.71226

    Figure Lengend Snippet: (A) Glioma cell survival at 24 h after SS treatment. (B) Glioma cell survival after pretreatment with DFO, FAC, Fer‐1, and Lip‐1, respectively, for 1 h before SS treatment. (C–F) Intracellular ROS, MDA, GSH/GSSG, and ferrous ion levels at 6, 12, and 24 h after SS treatment, with and without DFO, Fer‐1, Lip‐1, and FAC pretreatment for 1 h before SS treatment, respectively. (G) Glioma cell survival after SS treatment, with and without pretreatment with NAC and GSH for 1 h before SS treatment, respectively. (H) Western blots of ferroptosis‐related protein expression after SS treatment. Cell survival was assessed by the CCK‐8 assay. (I) Western blots of ATF3 expression in the cytoplasm and nuclei of SS‐treated cells. (J) Viability of cells treated with siATF3 followed by SS. (K–N) Ferrous ion, MDA, GSH/GSSG, and ROS levels in cells treated with siATF3 followed by SS. (O) Confocal microscopic images of ATF3 immunofluorescence in U251 cells treated with SS. (P, Q) Confocal microscopy images and fluorescence intensity measurements of mitochondrial superoxide in SS‐ and siATF3‐treated U251 and T98 cells. * p < 0.01 versus control, # p < 0.01 versus treatment group.

    Article Snippet: SS and cell counting kit‐8 (CCK‐8) kits were purchased from TargetMol (China).

    Techniques: Western Blot, Expressing, CCK-8 Assay, Confocal, Immunofluorescence, Microscopy, Fluorescence, Control