Journal: Communications Biology

Article Title: TRIM21 promotes K63-linked ubiquitination of ALKBH5 and suppresses cuproptosis via down-regulation of LIAS in esophageal squamous cell carcinoma

doi: 10.1038/s42003-025-09201-6

Figure Lengend Snippet: A Heat map illustrating genes downregulated upon ALKBH5 overexpression detected by RNA sequencing. B KEGG pathway analysis of differentially expressed genes (logFC > 1). C GSEA analysis confirmed significant correlations between RNA degradation pathways and ALKBH5 expression. D RNA Immunoprecipitation (RIP) of ALKBH5 followed by qRT-PCR ( n = 3 independent experiments). E RNA Immunoprecipitation (RIP) of ALKBH5 followed by PCR. F qRT-PCR assays for RNA stability showed that knocking down TRIM21 increased LIAS mRNA stability ( n = 3 independent experiments). G qRT-PCR assays for RNA stability showed that knocking down ALKBH5 increased LIAS mRNA stability ( n = 3 independent experiments). H Measurement of m6A modification levels on LIAS through m6A-IP after knocking down or overexpression of TRIM21 ( n = 3 independent experiments). I Measurement of m6A modification levels on LIAS through m6A-IP after knocking down or overexpression of ALKBH5 ( n = 3 independent experiments). J RIP-qPCR for IGF2BP3 revealed binding of LIAS mRNA to IGF2BP3 ( n = 3 independent experiments). K Knocking down IGF2BP3 notably decreased both the RNA expression levels of LIAS, and this effect was partially rescued by concurrent knockdown of ALKBH5 ( n = 3 independent experiments). L Knocking down IGF2BP3 notably decreased both the protein levels of LIAS, and this effect was partially rescued by concurrent knockdown of ALKBH5 ( n = 3 independent experiments). M qRT-PCR showed LIAS mRNA stability was reduced after IGF2BP3 knockdown ( n = 3 independent experiments). Error bars indicate standard deviations (ns: none significant; * p < 0.05; ** p < 0.01; *** p < 0.001).

Article Snippet: After dewaxing and hydration, the sections were incubated overnight with Abs against human TRIM21 (12108-1-AP; Proteintech; concentration: 1:500), human LIAS (11577-1-AP; Proteintech; concentration: 1:200), Ki-67 (9129; Cell Signaling Technology; concentration: 1:1000), human ALKBH5 (16837-1-AP; Proteintech; concentration: 1:500), DYKDDDDK Tag (14793; Cell Signaling Technology; concentration: 1:500), Myc-Tag (2278; Cell Signaling Technology; concentration: 1:500).

Techniques: Over Expression, RNA Sequencing, Expressing, RNA Immunoprecipitation, Quantitative RT-PCR, Modification, Binding Assay, RNA Expression, Knockdown

Journal: Communications Biology

Article Title: TRIM21 promotes K63-linked ubiquitination of ALKBH5 and suppresses cuproptosis via down-regulation of LIAS in esophageal squamous cell carcinoma

doi: 10.1038/s42003-025-09201-6

Figure Lengend Snippet: A Western blot showing knockdown of TRIM21 significantly increased LIAS expression without affecting ALKBH5 expression. B Nuclear and cytoplasmic fractionation assays followed by Western Blot analysis showed decreased ALKBH5 nuclear localization upon TRIM21 knockdown. C Immunofluorescence staining (IF) demonstrating that knockdown of TRIM21 supresses the nucleocytoplasmic trafficking of ALKBH5. D Apoptosis experiments illustrated that ESCC cells knockdown of TRIM21 or ALKBH5 both increased the sensitivity of cells to cuproptosis, while simultaneous knockout of LIAS attenuated or even counteracted this effect. E CCK8 assays showing that knockdown of TRIM21 inhibited the viability of tumor cells under elesclomol-Cu 2+ stimulation, and this effect could be reversed by LIAS knockdown ( n = 3 independent experiments). F CCK8 assays showing that ESCC cells became more susceptible to elesclomol-Cu 2+ -induced cuproptosis after mutation on ubiquitination site K147 (K147R) compared to Wild Type (WT) ( n = 3 independent experiments). Error bars indicate standard deviations (ns: none significant; * p < 0.05; ** p < 0.01; *** p < 0.001).

Article Snippet: After dewaxing and hydration, the sections were incubated overnight with Abs against human TRIM21 (12108-1-AP; Proteintech; concentration: 1:500), human LIAS (11577-1-AP; Proteintech; concentration: 1:200), Ki-67 (9129; Cell Signaling Technology; concentration: 1:1000), human ALKBH5 (16837-1-AP; Proteintech; concentration: 1:500), DYKDDDDK Tag (14793; Cell Signaling Technology; concentration: 1:500), Myc-Tag (2278; Cell Signaling Technology; concentration: 1:500).

Techniques: Western Blot, Knockdown, Expressing, Fractionation, Immunofluorescence, Staining, Knock-Out, Mutagenesis, Ubiquitin Proteomics

Journal: Communications Biology

Article Title: TRIM21 promotes K63-linked ubiquitination of ALKBH5 and suppresses cuproptosis via down-regulation of LIAS in esophageal squamous cell carcinoma

doi: 10.1038/s42003-025-09201-6

Figure Lengend Snippet: A Subcutaneous xenograft tumor model in nude mice using the esophageal squamous cell carcinoma cell line ECA109, mice were injected with elesclomol in both control (Ctrl) and TRIM21 knockdown (shTRIM21) groups. B Tumor sizes and weights are depicted in the figure ( n = 4 independent experiments). C Proteins from the tumor tissues were extracted for Western Blot analysis, which revealed TRIM21, LIAS protein expression levels. D RNA from the tumor tissues was extracted for qRT-PCR analysis, which revealed TRIM21, LIAS, ALKBH5 mRNA expression levels ( n = 3 independent experiments). E Immunostaining for TRIM21, Ki-67, and TUNEL was performed across the groups. F Quantification of ( E ) ( n = 3 independent experiments). Error bars indicate standard deviations (ns: none significant; * p < 0.05; ** p < 0.01; *** p < 0.001).

Article Snippet: After dewaxing and hydration, the sections were incubated overnight with Abs against human TRIM21 (12108-1-AP; Proteintech; concentration: 1:500), human LIAS (11577-1-AP; Proteintech; concentration: 1:200), Ki-67 (9129; Cell Signaling Technology; concentration: 1:1000), human ALKBH5 (16837-1-AP; Proteintech; concentration: 1:500), DYKDDDDK Tag (14793; Cell Signaling Technology; concentration: 1:500), Myc-Tag (2278; Cell Signaling Technology; concentration: 1:500).

Techniques: Injection, Control, Knockdown, Western Blot, Expressing, Quantitative RT-PCR, Immunostaining, TUNEL Assay

Journal: Communications Biology

Article Title: TRIM21 promotes K63-linked ubiquitination of ALKBH5 and suppresses cuproptosis via down-regulation of LIAS in esophageal squamous cell carcinoma

doi: 10.1038/s42003-025-09201-6

Figure Lengend Snippet: A Co-immunoprecipitation assays revealing that OGT and ALKBH5 can interact with each other. B Myc-OGT plasmid, along with HA-UB and Flag-ALKBH5, was transfected into HEK-293T cells, western blot showed overexpression of myc-OGT promoted the ubiquitination of ALKBH5. C Western blot showing co-transfection of TRIM21 with OGT augmented ALKBH5 ubiquitination. D Co-IP followed by western blot showing overexpression of OGT led to an increase in O-glycosylation of ALKBH5. E Co-IP followed by western blot showing knockdown of OGT led to the decrease in the binding of ALKBH5 and TRIM21, also induced upregulation of LIAS. F Co-IP followed by western blot analysis showing reduced ALKBH5 O-glycosylation and interaction with TRIM21 upon introducing the OGT inhibitor OSMI-1 in different concentrations. G A significant negative correlation in protein expression between the co-expression of OGT and TRIM21 with LIAS, Lipoylated-DLAT (Lip-DLAT), and Lipoylated-DLST (Lip-DLST) expression was observed by western blot, upon OSMI-1 treatment, the expressions of Lip-DLAT, Lip-DLST, and LIAS were restored. H Protein expression showing negative correlation between OGT and TRIM21 with LIAS, Lipoylated-DLAT (Lip-DLAT), and Lipoylated-DLST (Lip-DLST) after OGT or TRIM21 knockdown. I Following treatment with a gradient of OSMI-1 concentrations, nuclear-cytoplasmic fractionation experiments showed that OSMI-1 inhibited ALKBH5's accumulation in the nucleus.

Article Snippet: After dewaxing and hydration, the sections were incubated overnight with Abs against human TRIM21 (12108-1-AP; Proteintech; concentration: 1:500), human LIAS (11577-1-AP; Proteintech; concentration: 1:200), Ki-67 (9129; Cell Signaling Technology; concentration: 1:1000), human ALKBH5 (16837-1-AP; Proteintech; concentration: 1:500), DYKDDDDK Tag (14793; Cell Signaling Technology; concentration: 1:500), Myc-Tag (2278; Cell Signaling Technology; concentration: 1:500).

Techniques: Immunoprecipitation, Plasmid Preparation, Transfection, Western Blot, Over Expression, Ubiquitin Proteomics, Cotransfection, Co-Immunoprecipitation Assay, Glycoproteomics, Knockdown, Binding Assay, Expressing, Fractionation

Journal: Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography

Article Title: Therapeutic Ultrasound Increases Myocardial Blood Flow in Ischemic Myocardium and Cardiac Endothelial Cells: Results of In-vivo and In-Vitro Experiments

doi: 10.1016/j.echo.2019.05.012

Figure Lengend Snippet: MCE images from a control dog. Panels A to C depict LAD perfusion bed size, risk area, and ROI’s placed over the myocardium at baseline MCE image (stage A) from where time versus acoustic intensity plots were derived. Panels D and E depict the actual plots derived from the risk area and border zone during coronary occlusion (stage B) and 45 min after treatment period (stage D). Videos 1 and 2 depict the MCE aligned end-systolic images at different PI’s from where the plots were derived at stages B and D, respectively. See text for details.

Article Snippet: Similarly, US resulted in maintenance of transmural MBF in the border zone compared to control. table ft1 table-wrap mode="anchored" t5 Table 4. caption a7 Variables Stage A Stage B Stage C Stage D Stage E Myocardial Blood Volume (A)-Control 68±26 62±12 50±25 32±21 64±26 Myocardial Blood Volume (A)-US 82±13 61±24 61±15 58±26 64±19 MBF Velocity (β)-Control 0.44±0.19 0.27±0.20 0.22±0.12 0.29±0.19 0.30±0.14 MBF Velocity (β)-US 0.47±0.18 0.28±0.13 0.32±0.15 0.29±0.18 0.32±0.20 Total MBF (A·β)-Control 30±20 16±13 10±8 9±6 18±8 Total MBF (A·β)-US 37±12 17±10 20±10 * 15±8 19±13 Open in a separate window Stage A=baseline Stage B=LAD occlusion prior to treatment Stage C=LAD occlusion with or without treatment Stage D=LAD occlusion 45 min after treatment completion Stage E=90 min after reperfusion US=ultrasound; LAD=left anterior descending artery; MBF=myocardial blood flow; * p=0.03 MCE Results (mean±1SD) from the LAD Border Zone No changes were noted in any of the MCE parameters derived from the LCx bed between US and control groups at or between any of the stages.

Techniques: Derivative Assay

Journal: Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography

Article Title: Therapeutic Ultrasound Increases Myocardial Blood Flow in Ischemic Myocardium and Cardiac Endothelial Cells: Results of In-vivo and In-Vitro Experiments

doi: 10.1016/j.echo.2019.05.012

Figure Lengend Snippet: MCE images from a dog undergoing US treatment. Panels A to C depict LAD perfusion bed size, risk area, and ROI’s placed over the myocardium at baseline MCE image (stage A) from where time versus acoustic intensity plots were derived. Panels D and E depict the actual plots derived from the risk area and border zone during coronary occlusion (stage B) and 45 min after treatment period (stage D). Videos 3 and 4 depict the MCE aligned end-systolic images at different PI’s from where the plots were derived at stages B and D, respectively. See text for details.

Article Snippet: Similarly, US resulted in maintenance of transmural MBF in the border zone compared to control. table ft1 table-wrap mode="anchored" t5 Table 4. caption a7 Variables Stage A Stage B Stage C Stage D Stage E Myocardial Blood Volume (A)-Control 68±26 62±12 50±25 32±21 64±26 Myocardial Blood Volume (A)-US 82±13 61±24 61±15 58±26 64±19 MBF Velocity (β)-Control 0.44±0.19 0.27±0.20 0.22±0.12 0.29±0.19 0.30±0.14 MBF Velocity (β)-US 0.47±0.18 0.28±0.13 0.32±0.15 0.29±0.18 0.32±0.20 Total MBF (A·β)-Control 30±20 16±13 10±8 9±6 18±8 Total MBF (A·β)-US 37±12 17±10 20±10 * 15±8 19±13 Open in a separate window Stage A=baseline Stage B=LAD occlusion prior to treatment Stage C=LAD occlusion with or without treatment Stage D=LAD occlusion 45 min after treatment completion Stage E=90 min after reperfusion US=ultrasound; LAD=left anterior descending artery; MBF=myocardial blood flow; * p=0.03 MCE Results (mean±1SD) from the LAD Border Zone No changes were noted in any of the MCE parameters derived from the LCx bed between US and control groups at or between any of the stages.

Techniques: Derivative Assay

Journal: Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography

Article Title: Therapeutic Ultrasound Increases Myocardial Blood Flow in Ischemic Myocardium and Cardiac Endothelial Cells: Results of In-vivo and In-Vitro Experiments

doi: 10.1016/j.echo.2019.05.012

Figure Lengend Snippet: Hemodynamic Results (mean±1SD)

Article Snippet: Similarly, US resulted in maintenance of transmural MBF in the border zone compared to control. table ft1 table-wrap mode="anchored" t5 Table 4. caption a7 Variables Stage A Stage B Stage C Stage D Stage E Myocardial Blood Volume (A)-Control 68±26 62±12 50±25 32±21 64±26 Myocardial Blood Volume (A)-US 82±13 61±24 61±15 58±26 64±19 MBF Velocity (β)-Control 0.44±0.19 0.27±0.20 0.22±0.12 0.29±0.19 0.30±0.14 MBF Velocity (β)-US 0.47±0.18 0.28±0.13 0.32±0.15 0.29±0.18 0.32±0.20 Total MBF (A·β)-Control 30±20 16±13 10±8 9±6 18±8 Total MBF (A·β)-US 37±12 17±10 20±10 * 15±8 19±13 Open in a separate window Stage A=baseline Stage B=LAD occlusion prior to treatment Stage C=LAD occlusion with or without treatment Stage D=LAD occlusion 45 min after treatment completion Stage E=90 min after reperfusion US=ultrasound; LAD=left anterior descending artery; MBF=myocardial blood flow; * p=0.03 MCE Results (mean±1SD) from the LAD Border Zone No changes were noted in any of the MCE parameters derived from the LCx bed between US and control groups at or between any of the stages.

Techniques:

Journal: Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography

Article Title: Therapeutic Ultrasound Increases Myocardial Blood Flow in Ischemic Myocardium and Cardiac Endothelial Cells: Results of In-vivo and In-Vitro Experiments

doi: 10.1016/j.echo.2019.05.012

Figure Lengend Snippet: MCE Results (mean±1SD) from the LAD Risk Area

Article Snippet: Similarly, US resulted in maintenance of transmural MBF in the border zone compared to control. table ft1 table-wrap mode="anchored" t5 Table 4. caption a7 Variables Stage A Stage B Stage C Stage D Stage E Myocardial Blood Volume (A)-Control 68±26 62±12 50±25 32±21 64±26 Myocardial Blood Volume (A)-US 82±13 61±24 61±15 58±26 64±19 MBF Velocity (β)-Control 0.44±0.19 0.27±0.20 0.22±0.12 0.29±0.19 0.30±0.14 MBF Velocity (β)-US 0.47±0.18 0.28±0.13 0.32±0.15 0.29±0.18 0.32±0.20 Total MBF (A·β)-Control 30±20 16±13 10±8 9±6 18±8 Total MBF (A·β)-US 37±12 17±10 20±10 * 15±8 19±13 Open in a separate window Stage A=baseline Stage B=LAD occlusion prior to treatment Stage C=LAD occlusion with or without treatment Stage D=LAD occlusion 45 min after treatment completion Stage E=90 min after reperfusion US=ultrasound; LAD=left anterior descending artery; MBF=myocardial blood flow; * p=0.03 MCE Results (mean±1SD) from the LAD Border Zone No changes were noted in any of the MCE parameters derived from the LCx bed between US and control groups at or between any of the stages.

Techniques:

Journal: Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography

Article Title: Therapeutic Ultrasound Increases Myocardial Blood Flow in Ischemic Myocardium and Cardiac Endothelial Cells: Results of In-vivo and In-Vitro Experiments

doi: 10.1016/j.echo.2019.05.012

Figure Lengend Snippet: MCE Results (mean±1SD) from the LAD Border Zone

Article Snippet: Similarly, US resulted in maintenance of transmural MBF in the border zone compared to control. table ft1 table-wrap mode="anchored" t5 Table 4. caption a7 Variables Stage A Stage B Stage C Stage D Stage E Myocardial Blood Volume (A)-Control 68±26 62±12 50±25 32±21 64±26 Myocardial Blood Volume (A)-US 82±13 61±24 61±15 58±26 64±19 MBF Velocity (β)-Control 0.44±0.19 0.27±0.20 0.22±0.12 0.29±0.19 0.30±0.14 MBF Velocity (β)-US 0.47±0.18 0.28±0.13 0.32±0.15 0.29±0.18 0.32±0.20 Total MBF (A·β)-Control 30±20 16±13 10±8 9±6 18±8 Total MBF (A·β)-US 37±12 17±10 20±10 * 15±8 19±13 Open in a separate window Stage A=baseline Stage B=LAD occlusion prior to treatment Stage C=LAD occlusion with or without treatment Stage D=LAD occlusion 45 min after treatment completion Stage E=90 min after reperfusion US=ultrasound; LAD=left anterior descending artery; MBF=myocardial blood flow; * p=0.03 MCE Results (mean±1SD) from the LAD Border Zone No changes were noted in any of the MCE parameters derived from the LCx bed between US and control groups at or between any of the stages.

Techniques:

Journal: Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography

Article Title: Therapeutic Ultrasound Increases Myocardial Blood Flow in Ischemic Myocardium and Cardiac Endothelial Cells: Results of In-vivo and In-Vitro Experiments

doi: 10.1016/j.echo.2019.05.012

Figure Lengend Snippet: Regional Wall Thickening Results (mean±1SD)

Article Snippet: Similarly, US resulted in maintenance of transmural MBF in the border zone compared to control. table ft1 table-wrap mode="anchored" t5 Table 4. caption a7 Variables Stage A Stage B Stage C Stage D Stage E Myocardial Blood Volume (A)-Control 68±26 62±12 50±25 32±21 64±26 Myocardial Blood Volume (A)-US 82±13 61±24 61±15 58±26 64±19 MBF Velocity (β)-Control 0.44±0.19 0.27±0.20 0.22±0.12 0.29±0.19 0.30±0.14 MBF Velocity (β)-US 0.47±0.18 0.28±0.13 0.32±0.15 0.29±0.18 0.32±0.20 Total MBF (A·β)-Control 30±20 16±13 10±8 9±6 18±8 Total MBF (A·β)-US 37±12 17±10 20±10 * 15±8 19±13 Open in a separate window Stage A=baseline Stage B=LAD occlusion prior to treatment Stage C=LAD occlusion with or without treatment Stage D=LAD occlusion 45 min after treatment completion Stage E=90 min after reperfusion US=ultrasound; LAD=left anterior descending artery; MBF=myocardial blood flow; * p=0.03 MCE Results (mean±1SD) from the LAD Border Zone No changes were noted in any of the MCE parameters derived from the LCx bed between US and control groups at or between any of the stages.

Techniques:

Journal: Nutrients

Article Title: Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

doi: 10.3390/nu13061999

Figure Lengend Snippet: Effects of α-lipoic acid (LA) supplementation on body weight and nutritional profile.

Article Snippet: Animals were divided into three groups ( n = 8 in each): control pair-feeding group of rats fed a control diet (C) ( ); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (LA) (Chem Impex International, Inc., Wood Dale, USA, Cat# 29862) (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight).

Techniques:

Journal: Nutrients

Article Title: Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

doi: 10.3390/nu13061999

Figure Lengend Snippet: Effects of α-lipoic acid (LA) supplementation on: ( a ) liver/body weight ratio; ( b ) visceral adipose tissue (VAT)/body weight ratio. Animals were divided into three groups: control group of rats fed a control diet (C); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight). VAT: visceral (epididymal and retroperitoneal) adipose tissue. Values are mean ± standard error of the mean. p < 0.05 vs. * C.

Article Snippet: Animals were divided into three groups ( n = 8 in each): control pair-feeding group of rats fed a control diet (C) ( ); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (LA) (Chem Impex International, Inc., Wood Dale, USA, Cat# 29862) (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight).

Techniques:

Journal: Nutrients

Article Title: Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

doi: 10.3390/nu13061999

Figure Lengend Snippet: Effects of α-lipoic acid (LA) supplementation on liver lipid content.

Article Snippet: Animals were divided into three groups ( n = 8 in each): control pair-feeding group of rats fed a control diet (C) ( ); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (LA) (Chem Impex International, Inc., Wood Dale, USA, Cat# 29862) (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight).

Techniques:

Journal: Nutrients

Article Title: Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

doi: 10.3390/nu13061999

Figure Lengend Snippet: Effects of α-lipoic acid (LA) supplementation on plasma levels of ( a ) glucose, ( b ) triglycerides (TG), ( c ) free fatty acids (FFA), ( d ) total cholesterol (T-Chol), ( e ) high-density lipoprotein cholesterol (HDL-Chol), ( f ) low-density lipoprotein cholesterol (LDL-Chol). Animals were divided into three groups: control group of rats fed a control diet (C); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight). Values are mean ± standard error of the mean. p < 0.05 vs. * C; # HCCD+LA vs. HCCD.

Article Snippet: Animals were divided into three groups ( n = 8 in each): control pair-feeding group of rats fed a control diet (C) ( ); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (LA) (Chem Impex International, Inc., Wood Dale, USA, Cat# 29862) (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight).

Techniques:

Journal: Nutrients

Article Title: Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

doi: 10.3390/nu13061999

Figure Lengend Snippet: Effects of α-lipoic acid (LA) supplementation on ( a ) alanine aminotransferase (ALT) activity in plasma; ( b ) aspartate aminotransferase (AST) activity in plasma; ( c ) reduced glutathione (GSH) level in the liver; ( d ) reduced/oxidized glutathione ratio (GSH/GSSG) in the liver; ( e ) total antioxidant (AOA) activity in plasma; ( f ) total antioxidant (AOA) activity in the liver; ( g ) cytochrome P450 2E1 (CYP2E1) activity in the liver. Animals were divided into three groups: control group of rats fed a control diet (C); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight). Values are mean ± standard error of the mean. p < 0.05 vs. * C; # HCCD+LA vs. HCCD.

Article Snippet: Animals were divided into three groups ( n = 8 in each): control pair-feeding group of rats fed a control diet (C) ( ); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (LA) (Chem Impex International, Inc., Wood Dale, USA, Cat# 29862) (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight).

Techniques: Activity Assay

Journal: Nutrients

Article Title: Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

doi: 10.3390/nu13061999

Figure Lengend Snippet: Effects of α-lipoic acid (LA) supplementation on ( a ) catalase (CAT) activity in the liver; ( b ) glutathione peroxidase (GPx) activity in the liver; ( c ) superoxide dismutase (SOD) activity in the liver; ( d ) paraoxonase-1 (PON-1) activity in plasma; ( e ) paraoxonase-1 (PON-1) activity in the liver. Animals were divided into three groups: control group of rats fed a control diet (C); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight). Values are mean ± standard error of the mean. p < 0.05 vs. * C; # HCCD+LA vs. HCCD.

Article Snippet: Animals were divided into three groups ( n = 8 in each): control pair-feeding group of rats fed a control diet (C) ( ); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (LA) (Chem Impex International, Inc., Wood Dale, USA, Cat# 29862) (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight).

Techniques: Activity Assay

Journal: Nutrients

Article Title: Lipoic Acid Exacerbates Oxidative Stress and Lipid Accumulation in the Liver of Wistar Rats Fed a Hypercaloric Choline-Deficient Diet

doi: 10.3390/nu13061999

Figure Lengend Snippet: Effects of α-lipoic acid (LA) supplementation on histological features of the liver (portal area, ×100): ( a ) control group, hematoxylin-eosin stain; ( b ) control group, van Gieson stain; ( c ) hypercaloric choline-deficient diet group, hematoxylin-eosin stain; ( d ) hypercaloric choline-deficient diet group, van Gieson stain; ( e ) hypercaloric choline-deficient diet supplemented with α-lipoic acid (consumed average daily dose of LA-61 mg/kg body weight), hematoxylin-eosin stain; ( f ) hypercaloric choline-deficient diet supplemented with α-lipoic acid (consumed average daily dose of LA-61 mg/kg body weight), van Gieson stain. Large-sized lipid droplets are indicated by the blue arrow, foci of lobular inflammation by the black arrow, and hepatocellular ballooning by the red arrow. Scale bar = 500 μm.

Article Snippet: Animals were divided into three groups ( n = 8 in each): control pair-feeding group of rats fed a control diet (C) ( ); rats fed a hypercaloric choline-deficient diet (HCCD); rats fed a hypercaloric choline-deficient diet supplemented with α-lipoic acid (LA) (Chem Impex International, Inc., Wood Dale, USA, Cat# 29862) (HCCD+LA; consumed average daily dose of LA-61 mg/kg body weight).

Techniques: Staining