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human hepatocyte cell line thle 3  (ATCC)


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    ATCC human hepatocyte cell line thle 3
    Human Hepatocyte Cell Line Thle 3, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 301 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/human hepatocyte cell line thle 3/product/ATCC
    Average 96 stars, based on 301 article reviews
    human hepatocyte cell line thle 3 - by Bioz Stars, 2026-03
    96/100 stars

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    ATCC hepg2 human hepatic cell line
    Preclinical evaluation of QUINOLAM on metabolic and cellular endpoints in <t>HepG2</t> cells. ( A ) Cell viability assessed by MTT assay after 24 h exposure to increasing concentrations of QUINOLAM (0.003 to 1.6 mg/mL). No cytotoxic effects were observed up to 1.6 mg/mL. SDS (1 mg/mL) was used as a positive control. ( B ) Glucose uptake measured using the 2-NBDG fluorescent analog following 24 h treatment with QUINOLAM at 0.5, 1.0, and 2.5 mg/mL. A dose-dependent increase in glucose uptake was observed, with significant enhancement at 2.5 mg/mL ( p < 0.01 vs. control). ( C ) LDL receptor (LDL-R) protein expression determined by ELISA after 24 h exposure to QUINOLAM. Treatments with 1.0 and 2.5 mg/mL significantly upregulated LDL-R levels compared to untreated controls ( p < 0.05). ( D ) Antioxidant activity of QUINOLAM evaluated using the Trolox Equivalent Antioxidant Capacity (TEAC) assay. QUINOLAM displayed strong antioxidant potential in a dose-dependent manner, with significant increases in TEAC values at 0.1 and 0.2 mg/mL (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control). All data are expressed as mean ± standard deviation from three independent experiments.
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    ATCC human hepatocyte cell line thle3
    Preclinical evaluation of QUINOLAM on metabolic and cellular endpoints in <t>HepG2</t> cells. ( A ) Cell viability assessed by MTT assay after 24 h exposure to increasing concentrations of QUINOLAM (0.003 to 1.6 mg/mL). No cytotoxic effects were observed up to 1.6 mg/mL. SDS (1 mg/mL) was used as a positive control. ( B ) Glucose uptake measured using the 2-NBDG fluorescent analog following 24 h treatment with QUINOLAM at 0.5, 1.0, and 2.5 mg/mL. A dose-dependent increase in glucose uptake was observed, with significant enhancement at 2.5 mg/mL ( p < 0.01 vs. control). ( C ) LDL receptor (LDL-R) protein expression determined by ELISA after 24 h exposure to QUINOLAM. Treatments with 1.0 and 2.5 mg/mL significantly upregulated LDL-R levels compared to untreated controls ( p < 0.05). ( D ) Antioxidant activity of QUINOLAM evaluated using the Trolox Equivalent Antioxidant Capacity (TEAC) assay. QUINOLAM displayed strong antioxidant potential in a dose-dependent manner, with significant increases in TEAC values at 0.1 and 0.2 mg/mL (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control). All data are expressed as mean ± standard deviation from three independent experiments.
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    Average 96 stars, based on 1 article reviews
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    96/100 stars
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    ATCC cell culture 189 human hepatocyte cell line thle3
    Preclinical evaluation of QUINOLAM on metabolic and cellular endpoints in <t>HepG2</t> cells. ( A ) Cell viability assessed by MTT assay after 24 h exposure to increasing concentrations of QUINOLAM (0.003 to 1.6 mg/mL). No cytotoxic effects were observed up to 1.6 mg/mL. SDS (1 mg/mL) was used as a positive control. ( B ) Glucose uptake measured using the 2-NBDG fluorescent analog following 24 h treatment with QUINOLAM at 0.5, 1.0, and 2.5 mg/mL. A dose-dependent increase in glucose uptake was observed, with significant enhancement at 2.5 mg/mL ( p < 0.01 vs. control). ( C ) LDL receptor (LDL-R) protein expression determined by ELISA after 24 h exposure to QUINOLAM. Treatments with 1.0 and 2.5 mg/mL significantly upregulated LDL-R levels compared to untreated controls ( p < 0.05). ( D ) Antioxidant activity of QUINOLAM evaluated using the Trolox Equivalent Antioxidant Capacity (TEAC) assay. QUINOLAM displayed strong antioxidant potential in a dose-dependent manner, with significant increases in TEAC values at 0.1 and 0.2 mg/mL (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control). All data are expressed as mean ± standard deviation from three independent experiments.
    Cell Culture 189 Human Hepatocyte Cell Line Thle3, supplied by ATCC, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Preclinical evaluation of QUINOLAM on metabolic and cellular endpoints in HepG2 cells. ( A ) Cell viability assessed by MTT assay after 24 h exposure to increasing concentrations of QUINOLAM (0.003 to 1.6 mg/mL). No cytotoxic effects were observed up to 1.6 mg/mL. SDS (1 mg/mL) was used as a positive control. ( B ) Glucose uptake measured using the 2-NBDG fluorescent analog following 24 h treatment with QUINOLAM at 0.5, 1.0, and 2.5 mg/mL. A dose-dependent increase in glucose uptake was observed, with significant enhancement at 2.5 mg/mL ( p < 0.01 vs. control). ( C ) LDL receptor (LDL-R) protein expression determined by ELISA after 24 h exposure to QUINOLAM. Treatments with 1.0 and 2.5 mg/mL significantly upregulated LDL-R levels compared to untreated controls ( p < 0.05). ( D ) Antioxidant activity of QUINOLAM evaluated using the Trolox Equivalent Antioxidant Capacity (TEAC) assay. QUINOLAM displayed strong antioxidant potential in a dose-dependent manner, with significant increases in TEAC values at 0.1 and 0.2 mg/mL (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control). All data are expressed as mean ± standard deviation from three independent experiments.

    Journal: Medicina

    Article Title: Retrospective Analysis of a Quince, Olive Leaf, and Amaranth Nutraceutical in Patients with Metabolic Syndrome

    doi: 10.3390/medicina61091638

    Figure Lengend Snippet: Preclinical evaluation of QUINOLAM on metabolic and cellular endpoints in HepG2 cells. ( A ) Cell viability assessed by MTT assay after 24 h exposure to increasing concentrations of QUINOLAM (0.003 to 1.6 mg/mL). No cytotoxic effects were observed up to 1.6 mg/mL. SDS (1 mg/mL) was used as a positive control. ( B ) Glucose uptake measured using the 2-NBDG fluorescent analog following 24 h treatment with QUINOLAM at 0.5, 1.0, and 2.5 mg/mL. A dose-dependent increase in glucose uptake was observed, with significant enhancement at 2.5 mg/mL ( p < 0.01 vs. control). ( C ) LDL receptor (LDL-R) protein expression determined by ELISA after 24 h exposure to QUINOLAM. Treatments with 1.0 and 2.5 mg/mL significantly upregulated LDL-R levels compared to untreated controls ( p < 0.05). ( D ) Antioxidant activity of QUINOLAM evaluated using the Trolox Equivalent Antioxidant Capacity (TEAC) assay. QUINOLAM displayed strong antioxidant potential in a dose-dependent manner, with significant increases in TEAC values at 0.1 and 0.2 mg/mL (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 vs. control). All data are expressed as mean ± standard deviation from three independent experiments.

    Article Snippet: All in vitro experiments were conducted using the HepG2 human hepatic cell line (ATCC, Manassas, VA, USA).

    Techniques: MTT Assay, Positive Control, Control, Expressing, Enzyme-linked Immunosorbent Assay, Antioxidant Activity Assay, Standard Deviation