<p>HepG2 cells were treated CC-223 (500 nM) for 12 hours, mitochondrial depolarization (A) and ROS content (B) were tested. HepG2 cells were pretreated for 30 min with NAC (500 μM), MnTBAP (10 μM), cyclosporin A (CsA, 0.5 μM), or sanglifehrin A (SfA, 2.5 μM), followed by CC-223 (500 nM) treatment for indicated time period; Cell viability (CCK-8 assay, C) and cell apoptosis (TUNEL-nuclei staining assay, D) were tested. For each assay, n = 5. * <i>p</i> <0.05 <i>vs</i>. “C” (A and B). <sup>#</sup> <i>p</i> <0.05 <i>vs</i>. CC-223 only (C and D).</p
<p>HepG2 cells were treated with 0.6 mM H<sub>2</sub>O<sub>2</sub> for 8 h. (A) The percentage of ap...
<p>Cells were pretreated with a ROS scavenger (NAC), NADPH oxidase inhibitor (DPI), p38 inhibitor (S...
<p>(A) Shows the effects of DBPE (10μM), TBBPA (10μM), and HBCD (10μM) on mitochondrial membrane dep...
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related human mortalities. Over-activati...
<p>(A) Mean ROS levels in RCC4, untreated, CQ, CCI-779, or combination of CQ and CCI-779 after 6 hou...
<p>A. Cell vitality as determined by trypan blue (n = 4); B. Cell vitality as assessed by FACS (n = ...
In rat hepatocytes and isolated liver mitochondrial fractions, CsA is often used as a specific inhib...
<p>A. The MMP changes of HepG2 cells treated with DMQ (a) and H-EtOAc fraction (b). B. The productio...
<p><b>a)</b> Effect of MTBITC on ROS production in adherent growing cells. Cells were exposed to MTB...
<p>(A, B) The panels show representative images of DCFH-DA and HE accumulation in cells after UA tre...
<p>(A) Loss of mitochondrial membrane potential. Cells were incubated with AG–4 (5.4 μM, 0–48 h) and...
<p>HepG2-NS5A (<i>A</i>) and HepG2 control (<i>B</i>) cells were treated with 0–10 μM MG132 for 48 h...
<p>The standard cytotoxicity tests, including propidium iodide (PI)-based cell viability (A1–A3), MT...
<p><b>A.</b> LH86 and <b>B.</b> Huh7 cells were treated with ABT-263 (0–20 µM) for up to 24 h. Apopt...
<div><p>HepG2 cells were exposed to vehicle (DMSO, control), lithocholic (LCA, <b>A, C, E & F</b>), ...
<p>HepG2 cells were treated with 0.6 mM H<sub>2</sub>O<sub>2</sub> for 8 h. (A) The percentage of ap...
<p>Cells were pretreated with a ROS scavenger (NAC), NADPH oxidase inhibitor (DPI), p38 inhibitor (S...
<p>(A) Shows the effects of DBPE (10μM), TBBPA (10μM), and HBCD (10μM) on mitochondrial membrane dep...
Hepatocellular carcinoma (HCC) is a leading cause of cancer-related human mortalities. Over-activati...
<p>(A) Mean ROS levels in RCC4, untreated, CQ, CCI-779, or combination of CQ and CCI-779 after 6 hou...
<p>A. Cell vitality as determined by trypan blue (n = 4); B. Cell vitality as assessed by FACS (n = ...
In rat hepatocytes and isolated liver mitochondrial fractions, CsA is often used as a specific inhib...
<p>A. The MMP changes of HepG2 cells treated with DMQ (a) and H-EtOAc fraction (b). B. The productio...
<p><b>a)</b> Effect of MTBITC on ROS production in adherent growing cells. Cells were exposed to MTB...
<p>(A, B) The panels show representative images of DCFH-DA and HE accumulation in cells after UA tre...
<p>(A) Loss of mitochondrial membrane potential. Cells were incubated with AG–4 (5.4 μM, 0–48 h) and...
<p>HepG2-NS5A (<i>A</i>) and HepG2 control (<i>B</i>) cells were treated with 0–10 μM MG132 for 48 h...
<p>The standard cytotoxicity tests, including propidium iodide (PI)-based cell viability (A1–A3), MT...
<p><b>A.</b> LH86 and <b>B.</b> Huh7 cells were treated with ABT-263 (0–20 µM) for up to 24 h. Apopt...
<div><p>HepG2 cells were exposed to vehicle (DMSO, control), lithocholic (LCA, <b>A, C, E & F</b>), ...
<p>HepG2 cells were treated with 0.6 mM H<sub>2</sub>O<sub>2</sub> for 8 h. (A) The percentage of ap...
<p>Cells were pretreated with a ROS scavenger (NAC), NADPH oxidase inhibitor (DPI), p38 inhibitor (S...
<p>(A) Shows the effects of DBPE (10μM), TBBPA (10μM), and HBCD (10μM) on mitochondrial membrane dep...