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Liraglutide inhibits sensitivity of high glucose on ferroptosis. A Cell viability in HepG2 cells treated with indicated concentrations of high glucose (HG) for 24 h and 48 h. B Cell viability in Hep3B cells treated with HG (125 mM, 48 h) and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h) . Bar graphs showing cell viability in indicated cells treated with HG (125 mM, 48 h) or erastin (10 µM, 24 h) (C) , RSL3 (1.0 µM, 24 h) D and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h). PLC cells viability were measured with 1 mM, 5 mM, 100 mM glucose (48 h) combined with erastin (24 h) E or RSL3 (24 h) (F) . G Cell viability measured in HepG2 cells treated with 125 mM HG and different concentrations of liraglutide for 48 h. H – I HepG2 and Hep3B cells were treated with 100 mM HG, erastin (5 μM) and combined with 1.0 μM liraglutide for 24 h. J , K HepG2 and Hep3B cells were treated with 100 mM HG, RSL3 (0.5 μM) and combined with 1.0 μM liragluide for 24 h. Cell viability was determined by <t>CCK-8</t> assays. L Cell viability measured in HepG2 cells treated with different concentrations of erastin (24 h) combined with 2.0 μM liraglutide (48 h). M Cell viability measured in HepG2 cells treated with different concentrations of RSL3 (24 h) combined with 2.0 μM liraglutide (48 h). N Representative images from immunohistochemical staining of liver tissue microarray for Cleaved caspase-3 and 4-HNE (scale bar, 50 μm). O Representative Fe 2+ fluorescence images of HepG2 cell (scale bar, 100 μm) Data are expressed as mean ± SD, n = 4
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Promega cell counting kit-8 solution (cck-8)
Liraglutide inhibits sensitivity of high glucose on ferroptosis. A Cell viability in HepG2 cells treated with indicated concentrations of high glucose (HG) for 24 h and 48 h. B Cell viability in Hep3B cells treated with HG (125 mM, 48 h) and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h) . Bar graphs showing cell viability in indicated cells treated with HG (125 mM, 48 h) or erastin (10 µM, 24 h) (C) , RSL3 (1.0 µM, 24 h) D and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h). PLC cells viability were measured with 1 mM, 5 mM, 100 mM glucose (48 h) combined with erastin (24 h) E or RSL3 (24 h) (F) . G Cell viability measured in HepG2 cells treated with 125 mM HG and different concentrations of liraglutide for 48 h. H – I HepG2 and Hep3B cells were treated with 100 mM HG, erastin (5 μM) and combined with 1.0 μM liraglutide for 24 h. J , K HepG2 and Hep3B cells were treated with 100 mM HG, RSL3 (0.5 μM) and combined with 1.0 μM liragluide for 24 h. Cell viability was determined by <t>CCK-8</t> assays. L Cell viability measured in HepG2 cells treated with different concentrations of erastin (24 h) combined with 2.0 μM liraglutide (48 h). M Cell viability measured in HepG2 cells treated with different concentrations of RSL3 (24 h) combined with 2.0 μM liraglutide (48 h). N Representative images from immunohistochemical staining of liver tissue microarray for Cleaved caspase-3 and 4-HNE (scale bar, 50 μm). O Representative Fe 2+ fluorescence images of HepG2 cell (scale bar, 100 μm) Data are expressed as mean ± SD, n = 4
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Liraglutide inhibits sensitivity of high glucose on ferroptosis. A Cell viability in HepG2 cells treated with indicated concentrations of high glucose (HG) for 24 h and 48 h. B Cell viability in Hep3B cells treated with HG (125 mM, 48 h) and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h) . Bar graphs showing cell viability in indicated cells treated with HG (125 mM, 48 h) or erastin (10 µM, 24 h) (C) , RSL3 (1.0 µM, 24 h) D and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h). PLC cells viability were measured with 1 mM, 5 mM, 100 mM glucose (48 h) combined with erastin (24 h) E or RSL3 (24 h) (F) . G Cell viability measured in HepG2 cells treated with 125 mM HG and different concentrations of liraglutide for 48 h. H – I HepG2 and Hep3B cells were treated with 100 mM HG, erastin (5 μM) and combined with 1.0 μM liraglutide for 24 h. J , K HepG2 and Hep3B cells were treated with 100 mM HG, RSL3 (0.5 μM) and combined with 1.0 μM liragluide for 24 h. Cell viability was determined by <t>CCK-8</t> assays. L Cell viability measured in HepG2 cells treated with different concentrations of erastin (24 h) combined with 2.0 μM liraglutide (48 h). M Cell viability measured in HepG2 cells treated with different concentrations of RSL3 (24 h) combined with 2.0 μM liraglutide (48 h). N Representative images from immunohistochemical staining of liver tissue microarray for Cleaved caspase-3 and 4-HNE (scale bar, 50 μm). O Representative Fe 2+ fluorescence images of HepG2 cell (scale bar, 100 μm) Data are expressed as mean ± SD, n = 4
Cell Counting Kit 8 (Wst 8 / Cck8) 1000test, supplied by Advisains, 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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Liraglutide inhibits sensitivity of high glucose on ferroptosis. A Cell viability in HepG2 cells treated with indicated concentrations of high glucose (HG) for 24 h and 48 h. B Cell viability in Hep3B cells treated with HG (125 mM, 48 h) and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h) . Bar graphs showing cell viability in indicated cells treated with HG (125 mM, 48 h) or erastin (10 µM, 24 h) (C) , RSL3 (1.0 µM, 24 h) D and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h). PLC cells viability were measured with 1 mM, 5 mM, 100 mM glucose (48 h) combined with erastin (24 h) E or RSL3 (24 h) (F) . G Cell viability measured in HepG2 cells treated with 125 mM HG and different concentrations of liraglutide for 48 h. H – I HepG2 and Hep3B cells were treated with 100 mM HG, erastin (5 μM) and combined with 1.0 μM liraglutide for 24 h. J , K HepG2 and Hep3B cells were treated with 100 mM HG, RSL3 (0.5 μM) and combined with 1.0 μM liragluide for 24 h. Cell viability was determined by <t>CCK-8</t> assays. L Cell viability measured in HepG2 cells treated with different concentrations of erastin (24 h) combined with 2.0 μM liraglutide (48 h). M Cell viability measured in HepG2 cells treated with different concentrations of RSL3 (24 h) combined with 2.0 μM liraglutide (48 h). N Representative images from immunohistochemical staining of liver tissue microarray for Cleaved caspase-3 and 4-HNE (scale bar, 50 μm). O Representative Fe 2+ fluorescence images of HepG2 cell (scale bar, 100 μm) Data are expressed as mean ± SD, n = 4
Wst, supplied by Danaher Inc, 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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U.S Everbright cell counting kit 8 cck8
Liraglutide inhibits sensitivity of high glucose on ferroptosis. A Cell viability in HepG2 cells treated with indicated concentrations of high glucose (HG) for 24 h and 48 h. B Cell viability in Hep3B cells treated with HG (125 mM, 48 h) and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h) . Bar graphs showing cell viability in indicated cells treated with HG (125 mM, 48 h) or erastin (10 µM, 24 h) (C) , RSL3 (1.0 µM, 24 h) D and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h). PLC cells viability were measured with 1 mM, 5 mM, 100 mM glucose (48 h) combined with erastin (24 h) E or RSL3 (24 h) (F) . G Cell viability measured in HepG2 cells treated with 125 mM HG and different concentrations of liraglutide for 48 h. H – I HepG2 and Hep3B cells were treated with 100 mM HG, erastin (5 μM) and combined with 1.0 μM liraglutide for 24 h. J , K HepG2 and Hep3B cells were treated with 100 mM HG, RSL3 (0.5 μM) and combined with 1.0 μM liragluide for 24 h. Cell viability was determined by <t>CCK-8</t> assays. L Cell viability measured in HepG2 cells treated with different concentrations of erastin (24 h) combined with 2.0 μM liraglutide (48 h). M Cell viability measured in HepG2 cells treated with different concentrations of RSL3 (24 h) combined with 2.0 μM liraglutide (48 h). N Representative images from immunohistochemical staining of liver tissue microarray for Cleaved caspase-3 and 4-HNE (scale bar, 50 μm). O Representative Fe 2+ fluorescence images of HepG2 cell (scale bar, 100 μm) Data are expressed as mean ± SD, n = 4
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ApexBio cell counting kit-8 (cck-8) assay
Liraglutide inhibits sensitivity of high glucose on ferroptosis. A Cell viability in HepG2 cells treated with indicated concentrations of high glucose (HG) for 24 h and 48 h. B Cell viability in Hep3B cells treated with HG (125 mM, 48 h) and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h) . Bar graphs showing cell viability in indicated cells treated with HG (125 mM, 48 h) or erastin (10 µM, 24 h) (C) , RSL3 (1.0 µM, 24 h) D and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h). PLC cells viability were measured with 1 mM, 5 mM, 100 mM glucose (48 h) combined with erastin (24 h) E or RSL3 (24 h) (F) . G Cell viability measured in HepG2 cells treated with 125 mM HG and different concentrations of liraglutide for 48 h. H – I HepG2 and Hep3B cells were treated with 100 mM HG, erastin (5 μM) and combined with 1.0 μM liraglutide for 24 h. J , K HepG2 and Hep3B cells were treated with 100 mM HG, RSL3 (0.5 μM) and combined with 1.0 μM liragluide for 24 h. Cell viability was determined by <t>CCK-8</t> assays. L Cell viability measured in HepG2 cells treated with different concentrations of erastin (24 h) combined with 2.0 μM liraglutide (48 h). M Cell viability measured in HepG2 cells treated with different concentrations of RSL3 (24 h) combined with 2.0 μM liraglutide (48 h). N Representative images from immunohistochemical staining of liver tissue microarray for Cleaved caspase-3 and 4-HNE (scale bar, 50 μm). O Representative Fe 2+ fluorescence images of HepG2 cell (scale bar, 100 μm) Data are expressed as mean ± SD, n = 4
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Image Search Results


Liraglutide inhibits sensitivity of high glucose on ferroptosis. A Cell viability in HepG2 cells treated with indicated concentrations of high glucose (HG) for 24 h and 48 h. B Cell viability in Hep3B cells treated with HG (125 mM, 48 h) and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h) . Bar graphs showing cell viability in indicated cells treated with HG (125 mM, 48 h) or erastin (10 µM, 24 h) (C) , RSL3 (1.0 µM, 24 h) D and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h). PLC cells viability were measured with 1 mM, 5 mM, 100 mM glucose (48 h) combined with erastin (24 h) E or RSL3 (24 h) (F) . G Cell viability measured in HepG2 cells treated with 125 mM HG and different concentrations of liraglutide for 48 h. H – I HepG2 and Hep3B cells were treated with 100 mM HG, erastin (5 μM) and combined with 1.0 μM liraglutide for 24 h. J , K HepG2 and Hep3B cells were treated with 100 mM HG, RSL3 (0.5 μM) and combined with 1.0 μM liragluide for 24 h. Cell viability was determined by CCK-8 assays. L Cell viability measured in HepG2 cells treated with different concentrations of erastin (24 h) combined with 2.0 μM liraglutide (48 h). M Cell viability measured in HepG2 cells treated with different concentrations of RSL3 (24 h) combined with 2.0 μM liraglutide (48 h). N Representative images from immunohistochemical staining of liver tissue microarray for Cleaved caspase-3 and 4-HNE (scale bar, 50 μm). O Representative Fe 2+ fluorescence images of HepG2 cell (scale bar, 100 μm) Data are expressed as mean ± SD, n = 4

Journal: Molecular Medicine

Article Title: Liraglutide attenuates type 2 diabetes mellitus-associated non-alcoholic fatty liver disease by activating AMPK/ACC signaling and inhibiting ferroptosis

doi: 10.1186/s10020-023-00721-7

Figure Lengend Snippet: Liraglutide inhibits sensitivity of high glucose on ferroptosis. A Cell viability in HepG2 cells treated with indicated concentrations of high glucose (HG) for 24 h and 48 h. B Cell viability in Hep3B cells treated with HG (125 mM, 48 h) and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h) . Bar graphs showing cell viability in indicated cells treated with HG (125 mM, 48 h) or erastin (10 µM, 24 h) (C) , RSL3 (1.0 µM, 24 h) D and combined with 5 µM Z-VAD-FMK (Z-VAD, 24 h), 2 µM Necrostatin-1 s (Nec-1 s, 24 h) and 5 µM ferrostatin-1 (Fer-1, 24 h). PLC cells viability were measured with 1 mM, 5 mM, 100 mM glucose (48 h) combined with erastin (24 h) E or RSL3 (24 h) (F) . G Cell viability measured in HepG2 cells treated with 125 mM HG and different concentrations of liraglutide for 48 h. H – I HepG2 and Hep3B cells were treated with 100 mM HG, erastin (5 μM) and combined with 1.0 μM liraglutide for 24 h. J , K HepG2 and Hep3B cells were treated with 100 mM HG, RSL3 (0.5 μM) and combined with 1.0 μM liragluide for 24 h. Cell viability was determined by CCK-8 assays. L Cell viability measured in HepG2 cells treated with different concentrations of erastin (24 h) combined with 2.0 μM liraglutide (48 h). M Cell viability measured in HepG2 cells treated with different concentrations of RSL3 (24 h) combined with 2.0 μM liraglutide (48 h). N Representative images from immunohistochemical staining of liver tissue microarray for Cleaved caspase-3 and 4-HNE (scale bar, 50 μm). O Representative Fe 2+ fluorescence images of HepG2 cell (scale bar, 100 μm) Data are expressed as mean ± SD, n = 4

Article Snippet: Cell viability was measured as described previously using the Cell Counting Kit-8 (CCK8) (Enogene, Nanjing, China).

Techniques: CCK-8 Assay, Immunohistochemistry, Staining, Microarray, Fluorescence