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cell culture conditions human fetal lung fibroblasts  (ATCC)


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    ATCC cell culture conditions human fetal lung fibroblasts
    Fig. 1. Effects of various concentrations of allicin with or without TGFβ1 on HFL-1-mediated collagen gel contraction and chemotaxis. <t>Fibroblasts</t> were grown in culture and mixed with three-dimensional collagen gels following treatment with various concentrations of allicin with or without TGFβ1 (a). The vertical axes show the collagen gel size on day 3 compared to that in the control. Fibroblasts were cultured and their response to fibronectin (20 μg/mL) was tested to evaluate chemotactic activity following treatment with various concentrations of allicin in the presence or absence of TGFβ1 (b). Vertical axes show the number of migrated cells in the five high-power fields. Data were evaluated by using one-way analysis of variance and are presented as mean ± SEM. *P < 0.05. 'v' represents the vehicle.
    Cell Culture Conditions Human Fetal Lung Fibroblasts, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 641 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cell+culture+conditions+human+fetal+lung+fibroblasts/pm40447631-96-10-22?v=ATCC
    Average 96 stars, based on 641 article reviews
    cell culture conditions human fetal lung fibroblasts - by Bioz Stars, 2026-08
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    1) Product Images from "Allicin induced AMPK signaling attenuated Smad3 pathway mediated lung fibrosis."

    Article Title: Allicin induced AMPK signaling attenuated Smad3 pathway mediated lung fibrosis.

    Journal: Scientific reports

    doi: 10.1038/s41598-025-01314-6

    Fig. 1. Effects of various concentrations of allicin with or without TGFβ1 on HFL-1-mediated collagen gel contraction and chemotaxis. Fibroblasts were grown in culture and mixed with three-dimensional collagen gels following treatment with various concentrations of allicin with or without TGFβ1 (a). The vertical axes show the collagen gel size on day 3 compared to that in the control. Fibroblasts were cultured and their response to fibronectin (20 μg/mL) was tested to evaluate chemotactic activity following treatment with various concentrations of allicin in the presence or absence of TGFβ1 (b). Vertical axes show the number of migrated cells in the five high-power fields. Data were evaluated by using one-way analysis of variance and are presented as mean ± SEM. *P < 0.05. 'v' represents the vehicle.
    Figure Legend Snippet: Fig. 1. Effects of various concentrations of allicin with or without TGFβ1 on HFL-1-mediated collagen gel contraction and chemotaxis. Fibroblasts were grown in culture and mixed with three-dimensional collagen gels following treatment with various concentrations of allicin with or without TGFβ1 (a). The vertical axes show the collagen gel size on day 3 compared to that in the control. Fibroblasts were cultured and their response to fibronectin (20 μg/mL) was tested to evaluate chemotactic activity following treatment with various concentrations of allicin in the presence or absence of TGFβ1 (b). Vertical axes show the number of migrated cells in the five high-power fields. Data were evaluated by using one-way analysis of variance and are presented as mean ± SEM. *P < 0.05. 'v' represents the vehicle.

    Techniques Used: Chemotaxis Assay, Control, Cell Culture, Activity Assay

    Fig. 5. Allicin suppressed lung fibrosis via AMPK signaling. Allicin suppressed the number of infiltrating macrophages in the acute inflammatory phase, resulting in suppression of the subsequent fibrosis phases induced by the lung fibroblast-mediated fibrotic processes. The efficacy of Allicin in alleviating lung fibroblast- mediated fibrosis was attributed to its ability to enhance AMPK signaling, which in turn suppressed the TGFβ1-induced canonical Smad3 pathways.
    Figure Legend Snippet: Fig. 5. Allicin suppressed lung fibrosis via AMPK signaling. Allicin suppressed the number of infiltrating macrophages in the acute inflammatory phase, resulting in suppression of the subsequent fibrosis phases induced by the lung fibroblast-mediated fibrotic processes. The efficacy of Allicin in alleviating lung fibroblast- mediated fibrosis was attributed to its ability to enhance AMPK signaling, which in turn suppressed the TGFβ1-induced canonical Smad3 pathways.

    Techniques Used:



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    ATCC cell culture conditions human fetal lung fibroblasts
    Fig. 1. Effects of various concentrations of allicin with or without TGFβ1 on HFL-1-mediated collagen gel contraction and chemotaxis. <t>Fibroblasts</t> were grown in culture and mixed with three-dimensional collagen gels following treatment with various concentrations of allicin with or without TGFβ1 (a). The vertical axes show the collagen gel size on day 3 compared to that in the control. Fibroblasts were cultured and their response to fibronectin (20 μg/mL) was tested to evaluate chemotactic activity following treatment with various concentrations of allicin in the presence or absence of TGFβ1 (b). Vertical axes show the number of migrated cells in the five high-power fields. Data were evaluated by using one-way analysis of variance and are presented as mean ± SEM. *P < 0.05. 'v' represents the vehicle.
    Cell Culture Conditions Human Fetal Lung Fibroblasts, supplied by ATCC, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cell+culture+conditions+human+fetal+lung+fibroblasts/pm40447631-96-10-22?v=ATCC
    Average 96 stars, based on 1 article reviews
    cell culture conditions human fetal lung fibroblasts - by Bioz Stars, 2026-08
    96/100 stars
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    Fig. 1. Effects of various concentrations of allicin with or without TGFβ1 on HFL-1-mediated collagen gel contraction and chemotaxis. Fibroblasts were grown in culture and mixed with three-dimensional collagen gels following treatment with various concentrations of allicin with or without TGFβ1 (a). The vertical axes show the collagen gel size on day 3 compared to that in the control. Fibroblasts were cultured and their response to fibronectin (20 μg/mL) was tested to evaluate chemotactic activity following treatment with various concentrations of allicin in the presence or absence of TGFβ1 (b). Vertical axes show the number of migrated cells in the five high-power fields. Data were evaluated by using one-way analysis of variance and are presented as mean ± SEM. *P < 0.05. 'v' represents the vehicle.

    Journal: Scientific reports

    Article Title: Allicin induced AMPK signaling attenuated Smad3 pathway mediated lung fibrosis.

    doi: 10.1038/s41598-025-01314-6

    Figure Lengend Snippet: Fig. 1. Effects of various concentrations of allicin with or without TGFβ1 on HFL-1-mediated collagen gel contraction and chemotaxis. Fibroblasts were grown in culture and mixed with three-dimensional collagen gels following treatment with various concentrations of allicin with or without TGFβ1 (a). The vertical axes show the collagen gel size on day 3 compared to that in the control. Fibroblasts were cultured and their response to fibronectin (20 μg/mL) was tested to evaluate chemotactic activity following treatment with various concentrations of allicin in the presence or absence of TGFβ1 (b). Vertical axes show the number of migrated cells in the five high-power fields. Data were evaluated by using one-way analysis of variance and are presented as mean ± SEM. *P < 0.05. 'v' represents the vehicle.

    Article Snippet: Scientific Reports | (2025) 15:19060 4| https://doi.org/10.1038/s41598-025-01314-6 Cell line and cell culture conditions Human fetal lung fibroblasts (HFL-1) were obtained from the American Type Culture Collection (CCL-153, Manassas, VA, USA) and cultured in DMEM supplemented with 10% FCS and 1% antibiotics.

    Techniques: Chemotaxis Assay, Control, Cell Culture, Activity Assay

    Fig. 5. Allicin suppressed lung fibrosis via AMPK signaling. Allicin suppressed the number of infiltrating macrophages in the acute inflammatory phase, resulting in suppression of the subsequent fibrosis phases induced by the lung fibroblast-mediated fibrotic processes. The efficacy of Allicin in alleviating lung fibroblast- mediated fibrosis was attributed to its ability to enhance AMPK signaling, which in turn suppressed the TGFβ1-induced canonical Smad3 pathways.

    Journal: Scientific reports

    Article Title: Allicin induced AMPK signaling attenuated Smad3 pathway mediated lung fibrosis.

    doi: 10.1038/s41598-025-01314-6

    Figure Lengend Snippet: Fig. 5. Allicin suppressed lung fibrosis via AMPK signaling. Allicin suppressed the number of infiltrating macrophages in the acute inflammatory phase, resulting in suppression of the subsequent fibrosis phases induced by the lung fibroblast-mediated fibrotic processes. The efficacy of Allicin in alleviating lung fibroblast- mediated fibrosis was attributed to its ability to enhance AMPK signaling, which in turn suppressed the TGFβ1-induced canonical Smad3 pathways.

    Article Snippet: Scientific Reports | (2025) 15:19060 4| https://doi.org/10.1038/s41598-025-01314-6 Cell line and cell culture conditions Human fetal lung fibroblasts (HFL-1) were obtained from the American Type Culture Collection (CCL-153, Manassas, VA, USA) and cultured in DMEM supplemented with 10% FCS and 1% antibiotics.

    Techniques: