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Effects of propofol intervention on oxidative stress and inflammatory factors in H/R‐stimulated cardiomyocytes. (A) Intracellular <t>malondialdehyde</t> <t>(MDA)</t> levels in H9c2 cells of each group determined by colorimetric kits. (B) ELISA detection of superoxide dismutase (SOD) expression in cells of each group. (C) Relative reactive oxygen species (ROS) contents in cells of each group measured using fluorescent probes. (D) ELISA quantification of tumor necrosis factor‐ α (TNF‐ α ) concentrations in cell culture supernatant of each group. (E) ELISA detection of interleukin‐6 (IL‐6) concentrations in cell culture supernatant of each group. (F) ELISA measurement of interleukin‐1 β (IL‐1 β ) concentrations in cell culture supernatant of each group. ∗∗ p < 0.01; ∗∗∗ p < 0.001.
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Effects of propofol intervention on oxidative stress and inflammatory factors in H/R‐stimulated cardiomyocytes. (A) Intracellular <t>malondialdehyde</t> <t>(MDA)</t> levels in H9c2 cells of each group determined by colorimetric kits. (B) ELISA detection of superoxide dismutase (SOD) expression in cells of each group. (C) Relative reactive oxygen species (ROS) contents in cells of each group measured using fluorescent probes. (D) ELISA quantification of tumor necrosis factor‐ α (TNF‐ α ) concentrations in cell culture supernatant of each group. (E) ELISA detection of interleukin‐6 (IL‐6) concentrations in cell culture supernatant of each group. (F) ELISA measurement of interleukin‐1 β (IL‐1 β ) concentrations in cell culture supernatant of each group. ∗∗ p < 0.01; ∗∗∗ p < 0.001.
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Effects of propofol intervention on oxidative stress and inflammatory factors in H/R‐stimulated cardiomyocytes. (A) Intracellular <t>malondialdehyde</t> <t>(MDA)</t> levels in H9c2 cells of each group determined by colorimetric kits. (B) ELISA detection of superoxide dismutase (SOD) expression in cells of each group. (C) Relative reactive oxygen species (ROS) contents in cells of each group measured using fluorescent probes. (D) ELISA quantification of tumor necrosis factor‐ α (TNF‐ α ) concentrations in cell culture supernatant of each group. (E) ELISA detection of interleukin‐6 (IL‐6) concentrations in cell culture supernatant of each group. (F) ELISA measurement of interleukin‐1 β (IL‐1 β ) concentrations in cell culture supernatant of each group. ∗∗ p < 0.01; ∗∗∗ p < 0.001.
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Effects of propofol intervention on oxidative stress and inflammatory factors in H/R‐stimulated cardiomyocytes. (A) Intracellular <t>malondialdehyde</t> <t>(MDA)</t> levels in H9c2 cells of each group determined by colorimetric kits. (B) ELISA detection of superoxide dismutase (SOD) expression in cells of each group. (C) Relative reactive oxygen species (ROS) contents in cells of each group measured using fluorescent probes. (D) ELISA quantification of tumor necrosis factor‐ α (TNF‐ α ) concentrations in cell culture supernatant of each group. (E) ELISA detection of interleukin‐6 (IL‐6) concentrations in cell culture supernatant of each group. (F) ELISA measurement of interleukin‐1 β (IL‐1 β ) concentrations in cell culture supernatant of each group. ∗∗ p < 0.01; ∗∗∗ p < 0.001.
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Knocking down HDAC4 inhibits glutamine metabolism in A549 cells. (A) Glutamine uptake levels in A549 cells. (B) Glutamate production levels in A549 cells. (C) α‐Ketoglutarate production levels in A549 cells. (D) Measurement of GLS activity in A549 cells. (E) DCFH‐DA staining was used to measure the level of ROS in cells. (F) A kit was used to measure <t>the</t> <t>GSH/GSSG</t> ratio. (G) Western blotting was used to detect the expression of Nrf2, HO‐1, and NQO1. ∗∗ p < 0.01, ∗∗∗ p < 0.001. Data are presented as mean ± SD. All experiments were performed with three independent biological replicates. Statistical analysis was conducted using Student’s t ‐test for panels (A)‒(G). GLS, glutaminase; DCFH‐DA, 2 ′ ,7 ′ dichlorodihydrofluorescein diacetate; ROS, reactive oxygen species; GSH, reduced glutathione; GSSG, oxidized glutathione; Nrf2, nuclear factor erythroid 2 related factor 2; HO‐1, heme oxygenase 1; NQO1: NAD(P)H quinone dehydrogenase 1. The original, uncropped western blot images for Figure are provided in the Supporting Information.
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Knocking down HDAC4 inhibits glutamine metabolism in A549 cells. (A) Glutamine uptake levels in A549 cells. (B) Glutamate production levels in A549 cells. (C) α‐Ketoglutarate production levels in A549 cells. (D) Measurement of GLS activity in A549 cells. (E) DCFH‐DA staining was used to measure the level of ROS in cells. (F) A kit was used to measure <t>the</t> <t>GSH/GSSG</t> ratio. (G) Western blotting was used to detect the expression of Nrf2, HO‐1, and NQO1. ∗∗ p < 0.01, ∗∗∗ p < 0.001. Data are presented as mean ± SD. All experiments were performed with three independent biological replicates. Statistical analysis was conducted using Student’s t ‐test for panels (A)‒(G). GLS, glutaminase; DCFH‐DA, 2 ′ ,7 ′ dichlorodihydrofluorescein diacetate; ROS, reactive oxygen species; GSH, reduced glutathione; GSSG, oxidized glutathione; Nrf2, nuclear factor erythroid 2 related factor 2; HO‐1, heme oxygenase 1; NQO1: NAD(P)H quinone dehydrogenase 1. The original, uncropped western blot images for Figure are provided in the Supporting Information.
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Knocking down HDAC4 inhibits glutamine metabolism in A549 cells. (A) Glutamine uptake levels in A549 cells. (B) Glutamate production levels in A549 cells. (C) α‐Ketoglutarate production levels in A549 cells. (D) Measurement of GLS activity in A549 cells. (E) DCFH‐DA staining was used to measure the level of ROS in cells. (F) A kit was used to measure <t>the</t> <t>GSH/GSSG</t> ratio. (G) Western blotting was used to detect the expression of Nrf2, HO‐1, and NQO1. ∗∗ p < 0.01, ∗∗∗ p < 0.001. Data are presented as mean ± SD. All experiments were performed with three independent biological replicates. Statistical analysis was conducted using Student’s t ‐test for panels (A)‒(G). GLS, glutaminase; DCFH‐DA, 2 ′ ,7 ′ dichlorodihydrofluorescein diacetate; ROS, reactive oxygen species; GSH, reduced glutathione; GSSG, oxidized glutathione; Nrf2, nuclear factor erythroid 2 related factor 2; HO‐1, heme oxygenase 1; NQO1: NAD(P)H quinone dehydrogenase 1. The original, uncropped western blot images for Figure are provided in the Supporting Information.
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Knocking down HDAC4 inhibits glutamine metabolism in A549 cells. (A) Glutamine uptake levels in A549 cells. (B) Glutamate production levels in A549 cells. (C) α‐Ketoglutarate production levels in A549 cells. (D) Measurement of GLS activity in A549 cells. (E) DCFH‐DA staining was used to measure the level of ROS in cells. (F) A kit was used to measure <t>the</t> <t>GSH/GSSG</t> ratio. (G) Western blotting was used to detect the expression of Nrf2, HO‐1, and NQO1. ∗∗ p < 0.01, ∗∗∗ p < 0.001. Data are presented as mean ± SD. All experiments were performed with three independent biological replicates. Statistical analysis was conducted using Student’s t ‐test for panels (A)‒(G). GLS, glutaminase; DCFH‐DA, 2 ′ ,7 ′ dichlorodihydrofluorescein diacetate; ROS, reactive oxygen species; GSH, reduced glutathione; GSSG, oxidized glutathione; Nrf2, nuclear factor erythroid 2 related factor 2; HO‐1, heme oxygenase 1; NQO1: NAD(P)H quinone dehydrogenase 1. The original, uncropped western blot images for Figure are provided in the Supporting Information.
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Knocking down HDAC4 inhibits glutamine metabolism in A549 cells. (A) Glutamine uptake levels in A549 cells. (B) Glutamate production levels in A549 cells. (C) α‐Ketoglutarate production levels in A549 cells. (D) Measurement of GLS activity in A549 cells. (E) DCFH‐DA staining was used to measure the level of ROS in cells. (F) A kit was used to measure <t>the</t> <t>GSH/GSSG</t> ratio. (G) Western blotting was used to detect the expression of Nrf2, HO‐1, and NQO1. ∗∗ p < 0.01, ∗∗∗ p < 0.001. Data are presented as mean ± SD. All experiments were performed with three independent biological replicates. Statistical analysis was conducted using Student’s t ‐test for panels (A)‒(G). GLS, glutaminase; DCFH‐DA, 2 ′ ,7 ′ dichlorodihydrofluorescein diacetate; ROS, reactive oxygen species; GSH, reduced glutathione; GSSG, oxidized glutathione; Nrf2, nuclear factor erythroid 2 related factor 2; HO‐1, heme oxygenase 1; NQO1: NAD(P)H quinone dehydrogenase 1. The original, uncropped western blot images for Figure are provided in the Supporting Information.
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Knocking down HDAC4 inhibits glutamine metabolism in A549 cells. (A) Glutamine uptake levels in A549 cells. (B) Glutamate production levels in A549 cells. (C) α‐Ketoglutarate production levels in A549 cells. (D) Measurement of GLS activity in A549 cells. (E) DCFH‐DA staining was used to measure the level of ROS in cells. (F) A kit was used to measure <t>the</t> <t>GSH/GSSG</t> ratio. (G) Western blotting was used to detect the expression of Nrf2, HO‐1, and NQO1. ∗∗ p < 0.01, ∗∗∗ p < 0.001. Data are presented as mean ± SD. All experiments were performed with three independent biological replicates. Statistical analysis was conducted using Student’s t ‐test for panels (A)‒(G). GLS, glutaminase; DCFH‐DA, 2 ′ ,7 ′ dichlorodihydrofluorescein diacetate; ROS, reactive oxygen species; GSH, reduced glutathione; GSSG, oxidized glutathione; Nrf2, nuclear factor erythroid 2 related factor 2; HO‐1, heme oxygenase 1; NQO1: NAD(P)H quinone dehydrogenase 1. The original, uncropped western blot images for Figure are provided in the Supporting Information.
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Effects of propofol intervention on oxidative stress and inflammatory factors in H/R‐stimulated cardiomyocytes. (A) Intracellular malondialdehyde (MDA) levels in H9c2 cells of each group determined by colorimetric kits. (B) ELISA detection of superoxide dismutase (SOD) expression in cells of each group. (C) Relative reactive oxygen species (ROS) contents in cells of each group measured using fluorescent probes. (D) ELISA quantification of tumor necrosis factor‐ α (TNF‐ α ) concentrations in cell culture supernatant of each group. (E) ELISA detection of interleukin‐6 (IL‐6) concentrations in cell culture supernatant of each group. (F) ELISA measurement of interleukin‐1 β (IL‐1 β ) concentrations in cell culture supernatant of each group. ∗∗ p < 0.01; ∗∗∗ p < 0.001.

Journal: Cardiovascular Therapeutics

Article Title: The miR‐511‐3p/ATP2A2 Axis Is Required for Propofol‐Mediated Cardioprotection Against Hypoxia/Reoxygenation Injury

doi: 10.1155/cdr/7021184

Figure Lengend Snippet: Effects of propofol intervention on oxidative stress and inflammatory factors in H/R‐stimulated cardiomyocytes. (A) Intracellular malondialdehyde (MDA) levels in H9c2 cells of each group determined by colorimetric kits. (B) ELISA detection of superoxide dismutase (SOD) expression in cells of each group. (C) Relative reactive oxygen species (ROS) contents in cells of each group measured using fluorescent probes. (D) ELISA quantification of tumor necrosis factor‐ α (TNF‐ α ) concentrations in cell culture supernatant of each group. (E) ELISA detection of interleukin‐6 (IL‐6) concentrations in cell culture supernatant of each group. (F) ELISA measurement of interleukin‐1 β (IL‐1 β ) concentrations in cell culture supernatant of each group. ∗∗ p < 0.01; ∗∗∗ p < 0.001.

Article Snippet: Colorimetric quantitative analysis was performed with lactate dehydrogenase (LDH) assay kits (Abcam, United Kingdom) and malondialdehyde (MDA) detection kits (Elabscience, China).

Techniques: Enzyme-linked Immunosorbent Assay, Expressing, Cell Culture

Knocking down HDAC4 inhibits glutamine metabolism in A549 cells. (A) Glutamine uptake levels in A549 cells. (B) Glutamate production levels in A549 cells. (C) α‐Ketoglutarate production levels in A549 cells. (D) Measurement of GLS activity in A549 cells. (E) DCFH‐DA staining was used to measure the level of ROS in cells. (F) A kit was used to measure the GSH/GSSG ratio. (G) Western blotting was used to detect the expression of Nrf2, HO‐1, and NQO1. ∗∗ p < 0.01, ∗∗∗ p < 0.001. Data are presented as mean ± SD. All experiments were performed with three independent biological replicates. Statistical analysis was conducted using Student’s t ‐test for panels (A)‒(G). GLS, glutaminase; DCFH‐DA, 2 ′ ,7 ′ dichlorodihydrofluorescein diacetate; ROS, reactive oxygen species; GSH, reduced glutathione; GSSG, oxidized glutathione; Nrf2, nuclear factor erythroid 2 related factor 2; HO‐1, heme oxygenase 1; NQO1: NAD(P)H quinone dehydrogenase 1. The original, uncropped western blot images for Figure are provided in the Supporting Information.

Journal: Analytical Cellular Pathology (Amsterdam)

Article Title: HDAC4 Promotes Cancer Stemness in Nonsmall Cell Lung Cancer by Upregulating SLC38A2 Expression via HIF‐1α to Enhance Glutamine Metabolism

doi: 10.1155/ancp/2525721

Figure Lengend Snippet: Knocking down HDAC4 inhibits glutamine metabolism in A549 cells. (A) Glutamine uptake levels in A549 cells. (B) Glutamate production levels in A549 cells. (C) α‐Ketoglutarate production levels in A549 cells. (D) Measurement of GLS activity in A549 cells. (E) DCFH‐DA staining was used to measure the level of ROS in cells. (F) A kit was used to measure the GSH/GSSG ratio. (G) Western blotting was used to detect the expression of Nrf2, HO‐1, and NQO1. ∗∗ p < 0.01, ∗∗∗ p < 0.001. Data are presented as mean ± SD. All experiments were performed with three independent biological replicates. Statistical analysis was conducted using Student’s t ‐test for panels (A)‒(G). GLS, glutaminase; DCFH‐DA, 2 ′ ,7 ′ dichlorodihydrofluorescein diacetate; ROS, reactive oxygen species; GSH, reduced glutathione; GSSG, oxidized glutathione; Nrf2, nuclear factor erythroid 2 related factor 2; HO‐1, heme oxygenase 1; NQO1: NAD(P)H quinone dehydrogenase 1. The original, uncropped western blot images for Figure are provided in the Supporting Information.

Article Snippet: The levels of total glutathione (T‐GSH) and GSSG in A549 cells were measured using a GSH/GSSG ratio detection kit (E‐BC‐K097‐M, Elabscience, China) following the manufacturer’s instructions.

Techniques: Activity Assay, Staining, Western Blot, Expressing, Analysis