Thrombopoietin Protects Cardiomyocytes from Iron-Overload Induced Oxidative Stress and Mitochondrial Injury

Chan, Stewart Siu-Wa; Chan, Godfrey Chi‐Fung; Ye, Jieyu; Lian, Qizhou; Chen, Jianliang; Yang, Mo

doi:10.1159/000430173

Cited by 24 publications

(16 citation statements)

References 26 publications

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“…PGC-1α, a coactivator of PPARγ, serves as an inducible booster involved in mitochondrial biogenesis [25,26]. In the current study, PGC-1α as well as its downstream effectors, including NRF1, TFAM and other related genes involved in NRF family was also found to be upregulated in cardiomyocytes after QLQX treatment at 0.5 μg/mL for 48 hours.…”

Section: Discussionsupporting

confidence: 55%

The Metabolic Effects of Traditional Chinese Medication Qiliqiangxin on H9C2 Cardiomyocytes

Lin¹,

Wu²,

Tao³

et al. 2015

Cell Physiol Biochem

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Background/Aims: A traditional Chinese medicine, Qiliqiangxin (QLQX) has been identified to perform protective effects on myocardium energy metabolism in mice with acute myocardial infarction, though the effects of QLQX on myocardial mitochondrial biogenesis under physiological condition is still largely elusive. Methods: H9C2 cells were treated with different concentrations of QLQX (0.25, 0.5, and 1.0 μg/mL) from 6 to 48 hours. Oxidative metabolism and glycolysis were measured by oxygen consumption and extracellular acidification with XF96 analyzer (SeaHorse). Mitochondrial content and ultrastructure were assessed by Mitotracker staining, confocal microscopy, flow cytometry, and transmission electron microscopy. Mitochondrial biogenesis-related genes were measured by qRT-PCR and Western blot. Results: H9C2 cells treated with QLQX exhibited increased glycolysis at earlier time points (6, 12, and 24 hours), while QLQX could enhance oxidative metabolism and mitochondrial uncoupling in H9C2 cells with longer duration of treatment (48 hours). QLQX also increased mitochondrial content and mitochondrial biogenesis-related gene expression levels, including 16sRNA, SSBP1, TWINKLE, TOP1MT and PLOG, with an activation of peroxisome proliferator-activated receptor coactivator 1 alpha (PGC-1α) and its downstream effectors. Silencing PGC-1α could abolish the increased mitochondrial content in H9C2 cells treated with QLQX. Conclusion: Our study is the first to document enhanced metabolism in cardiomyocytes treated with QLQX, which is linked to increased mitochondrial content and mitochondrial biogenesis via activation of PGC-1α.S. Lin, X. Wu and L. Tao contributed equally to this work.

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Section: Discussionsupporting

confidence: 55%

The Metabolic Effects of Traditional Chinese Medication Qiliqiangxin on H9C2 Cardiomyocytes

Lin¹,

Wu²,

Tao³

et al. 2015

Cell Physiol Biochem

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“…When the mitochondrial membrane potential becomes high, JC-1 forms a polymer that produces red fluorescence, while when the mitochondrial membrane potential is low, it produces a green fluorescence. This allows changes in the mitochondrial membrane potential to be detected by fluorescence color transitions [24,25]. In our results, the red fluorescence in the high-concentration H 2 O 2 injury group could be observed, the green fluorescence was significantly lower, and the ratio of red to green is 36.34 ± 5.62%, indicating that H 2 O 2 can decrease the mitochondrial membrane potential.…”

Section: Discussionsupporting

confidence: 49%

Preincubation with a low-dose hydrogen peroxide enhances anti-oxidative stress ability of BMSCs

et al. 2020

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Objective To investigate the effects of low-concentration hydrogen peroxide pretreatment on the anti-oxidative stress of the bone marrow mesenchymal stem cells (BMSCs). Methods Rabbit BMSCs were isolated and cultured by density gradient centrifugation combined with the adherence method. Then, the third generation of well-grown BMSCs was continuously treated with 50-μM hydrogen peroxide (H2O2) for 8 h as the optimal pretreatment concentration and the BMSCs were continuously applied for 24 h with 500 μM H2O2, and the optimal damage concentration was determined as the oxidative stress cell model. The experiment was divided into three groups: control group, high-concentration H2O2 injury group (500 μM), and low-concentration H2O2 pretreatment group (50 μM + 500 μM). In each group, the DCFH-DA fluorescence probe was used to detect the reactive oxygen species (ROS). ELISA was used to detect the activity of superoxide dismutase (SOD) and catalase (CAT), and the TBA method was used to detect malondialdehyde (MDA). The mitochondrial membrane potential was detected by JC-1. The cell viability was detected by CCK-8 method, while flow cytometry and TUNEL/DAPI double staining were performed to detect cell apoptosis. Hence, the effect of H2O2 pretreatment on the anti-oxidative stress of BMSCs was investigated. One-way analysis of variance was performed using SPSS 19.0 statistical software, and P < 0.05 was considered statistically significant. Results A large number of typical BMSCs were obtained by density gradient centrifugation and adherent culture. The oxidative stress cell model was successfully established by 500-μM H2O2. Compared with the high-concentration H2O2 injury group, the low-concentration H2O2 pretreatment reduced the production of ROS [(62.33 ± 5.05), P < 0.05], SOD and CAT activities significantly increased (P < 0.05), and MDA levels significantly decreased (P < 0.05). The mitochondrial membrane potential fluorescence changes, the ratio of red/green fluorescence intensity of the high-concentration H2O2 injury group was less, and the ratio of the low-concentration H2O2 pretreatment group was significantly higher than that. The ratio of red/green increased by about 1.8 times (P < 0.05). The cell viability and survival rate of BMSCs were significantly increased in low-concentration H2O2 pretreatment group (P < 0.05), and the cell apoptosis rate was significantly decreased (P < 0.05). Conclusion Pretreatment with low-concentration H2O2 can enhance the anti-oxidative stress ability and reduce their apoptosis of BMSCs under oxidative stress.

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“…The concentration of MDA can be measured by reacting with thiobarbituric acid (TBA) to form a stable chromophoric production. The MDA levels in the culture medium were measured by using an MDA assay kit (Jiancheng Bioengineering), as described previously [33]. The TBA method was used to analyze MDA by monitoring MDA-reactive products spectrophotometrically.…”

Section: Methodsmentioning

confidence: 99%

Aniline Induces Oxidative Stress and Apoptosis of Primary Cultured Hepatocytes

Wang

Gao

Xiaolin

et al. 2016

IJERPH

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The toxicity and carcinogenicity of aniline in humans and animals have been well documented. However, the molecular mechanism involved in aniline-induced liver toxicity and carcinogenesis remains unclear. In our research, primary cultured hepatocytes were exposed to aniline (0, 1.25, 2.50, 5.0 and 10.0 μg/mL) for 24 h in the presence or absence of N-acetyl-l-cysteine (NAC). Levels of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH), activities of superoxide dismutase (SOD) and catalase (CAT), mitochondrial membrane potential, DNA damage, cell viability, and apoptosis were detected. Levels of ROS and MDA were significantly increased and levels of GSH and CAT, activity of SOD, and mitochondrial membrane potential in hepatocytes were significantly decreased by aniline compared with the negative control group. The tail moment and DNA content of the tail in exposed groups were significantly higher than those in the negative control group. Cell viability was reduced and apoptotic death was induced by aniline in a concentration-dependent manner. The phenomena of ROS generation, oxidative damage, loss of mitochondrial membrane potential, DNA damage and apoptosis could be prevented if ROS inhibitor NAC was added. ROS generation is involved in the loss of mitochondrial membrane potential and DNA injury, which may play a role in aniline-induced apoptosis in hepatocytes. Our study provides insight into the mechanism of aniline-induced toxicity and apoptosis of hepatocytes.

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Thrombopoietin Protects Cardiomyocytes from Iron-Overload Induced Oxidative Stress and Mitochondrial Injury

Cited by 24 publications

References 26 publications

The Metabolic Effects of Traditional Chinese Medication Qiliqiangxin on H9C2 Cardiomyocytes

The Metabolic Effects of Traditional Chinese Medication Qiliqiangxin on H9C2 Cardiomyocytes

Preincubation with a low-dose hydrogen peroxide enhances anti-oxidative stress ability of BMSCs

Aniline Induces Oxidative Stress and Apoptosis of Primary Cultured Hepatocytes

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