Astragalus Salvia Granules to Benefit the Qi (Qishen Yiqi Keli) protects H9C2 cardiomyocytes by suppressing oxidative stress

Background/Aims: The myocardial energy metabolism shift is one of the most important pathological features of ischemic heart disease (IHD). Although several microRNAs (miRs) are involved in the regulation of myocardial energy metabolism, their exact effects and underlying mechanisms remain unclear. The aim of this study was to investigate whether microRNA(miR-210) regulates the energy metabolism shift during oxidative stress in H9c2 cardiomyocytes. Methods: Cell survival was analyzed via CCK assay. The energy metabolism shift was detected by lactate assay, ATP assay and RT2 profiler glucose metabolism PCR array. Protein and mRNA expression levels were determined by western blot and qPCR. We also used kits to detect the activity of Complex I, Sirt3 and the NAD+/NADH ratio. Results: We determined that miR-210 promoted the energy metabolism shift. The iron-sulfur cluster assembly protein (ISCU) was a target of miR-210. Additionally, we detected the activity of complex I and found that miR-210 inhibits mitochondrial respiration. Interestingly, miR-210 may also indirectly regulate SIRT3 by regulating ISCU. Conclusion: Our results confirm that miR-210 is essential and sufficient for modulating the cellular energy metabolism shift during H2O2-induced oxidative stress in H9c2 cardiomyocytes by targeting ISCU.

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Sodium Tanshinone IIA Sulfonate Prevents Radiation-Induced Toxicity in H9c2 Cardiomyocytes

Evidence-based Complementary and Alternative Medicine ◽

10.1155/2017/4537974 ◽

2017 ◽

Vol 2017 ◽

pp. 1-13 ◽

Cited By ~ 4

Author(s):

Wenjing Zhang ◽

Yi Li ◽

Rui Li ◽

Yaya Wang ◽

Mengwen Zhu ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Cycle ◽

Antioxidant Activity ◽

Cell Cycle Arrest ◽

Tanshinone Iia ◽

H9c2 Cells ◽

X Ray ◽

Cycle Arrest ◽

H9c2 Cardiomyocytes ◽

Radiation Induced

The present study was designed to elucidate the key parameters associated with X-ray radiation induced oxidative stress and the effects of STS on X-ray-induced toxicity in H9c2 cardiomyocytes. Cytotoxicity of STS and radiation was assessed by MTT. Antioxidant activity was evaluated by SOD and MDA. Apoptosis was measured by the flow cytometry, Hoechst 33258, clonogenic survival assay, and western blot. It was found that the cell viability of H9c2 cells exposed to X-ray radiation was significantly decreased in a dose-dependent manner and was associated with cell cycle arrest at the G0/G1 phase as well as apoptosis. STS treatment significantly reversed the morphological changes, attenuated radiation-induced apoptosis, and improved the antioxidant activity in the H9c2 cells. STS significantly increased the Bcl-2 and Bcl-2/Bax levels and decreased the Bax and caspase-3 levels, compared with the cells treated with radiation alone. STS treatment also resulted in a significant increase in p38-MAPK activation. STS could protect the cells from X-ray-induced cell cycle arrest, oxidative stress, and apoptosis. Therefore, we suggest the STS could be useful for the treatment of radiation-induced cardiovascular injury.

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Aqueous extract of Cortex Dictamni protects H9c2 cardiomyocytes from hypoxia/reoxygenation-induced oxidative stress and apoptosis by PI3K/Akt signaling pathway

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2017.02.013 ◽

2017 ◽

Vol 89 ◽

pp. 233-244 ◽

Cited By ~ 15

Author(s):

Lin Li ◽

Yunfeng Zhou ◽

Yanlin Li ◽

Lili Wang ◽

Lan Sun ◽

...

Keyword(s):

Oxidative Stress ◽

Signaling Pathway ◽

Aqueous Extract ◽

Akt Signaling ◽

Akt Signaling Pathway ◽

H9c2 Cardiomyocytes ◽

Hypoxia Reoxygenation

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Palmitate-induced toxicity is associated with impaired mitochondrial respiration and accelerated oxidative stress in cultured cardiomyocytes: the critical role of Coenzyme Q9/10

10.1101/830331 ◽

2019 ◽

Author(s):

Phiwayinkosi V. Dludla ◽

Sonia Silvestri ◽

Patrick Orlando ◽

Sithandiwe E. Mazibuko-Mbeje ◽

Rabia Johnson ◽

...

Keyword(s):

Oxidative Stress ◽

Cell Viability ◽

Mitochondrial Function ◽

Mitochondrial Respiration ◽

Antioxidant Activities ◽

Critical Role ◽

Limited Information ◽

Transport Chain ◽

Oxidative Stress Status ◽

H9c2 Cardiomyocytes

AbstractImpaired mitochondrial function concomitant to enhanced oxidative stress-induced damage are well established mechanisms involved in hyperlipidemia-induced cardiotoxicity. Coenzyme Q9/10 (CoQ) is known to be a critical component of the mitochondrial electron transport chain that efficiently supports the process of bioenergetics in addition to its antioxidant activities. However, there is very limited information on the direct effect of myocardial lipid overload on endogenous CoQ levels in association with mitochondrial respiration and oxidative stress status. Here, such effects were explored by exposing H9c2 cardiomyocytes to various doses (0.15 to 1 mM) of palmitate for 24 hours. The results demonstrated that palmitate doses ≥ 0.25 mM are enough to impair mitochondrial respiration and cause oxidative stress. Although endogenous CoQ levels are enhanced by palmitate doses ≤ 5 mM, this is not enough to counteract oxidative stress, but is sufficient to maintain cell viability of cardiomyocytes, suggesting a compensation mechanism. Palmitate doses > 5 mM caused severe mitochondrial toxicity, including reduction of cell viability. Interestingly, enhancement of CoQ levels with the lowest dose of palmitate (0.15 mM) was accompanied by a significantly reduction of CoQ oxidation status, as well as low cytosolic production of reactive oxygen species. From the overall findings, it appears that CoQ response may be crucial to improve mitochondrial function and thus protect against hyperlipidemia-induced insult. These results further suggest that therapeutic agents that can stimulate endogenous levels of CoQ may be beneficial in protecting the myocardium against diabetes associated complications.

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Schisandrin B Antagonizes Cardiotoxicity Induced by Pirarubicin by Inhibiting Mitochondrial Permeability Transition Pore (mPTP) Opening and Decreasing Cardiomyocyte Apoptosis

Frontiers in Pharmacology ◽

10.3389/fphar.2021.733805 ◽

2021 ◽

Vol 12 ◽

Author(s):

Hongwei Shi ◽

Heng Tang ◽

Wen Ai ◽

Qingfu Zeng ◽

Hong Yang ◽

...

Keyword(s):

Oxidative Stress ◽

Mitochondrial Function ◽

Defense Mechanism ◽

Mitochondrial Permeability Transition ◽

Permeability Transition Pore ◽

Permeability Transition ◽

Mitochondrial Swelling ◽

Schisandrin B ◽

Mptp Opening ◽

H9c2 Cardiomyocytes

Objective: Pirarubicin (THP), one of the anthracycline anticancer drugs, is widely used in the treatment of various cancers, but its cardiotoxicity cannot be ignored. Schisandrin B (SchB) has the ability to upregulate cellular antioxidant defense mechanism and promote mitochondrial function and antioxidant status. However, it has not been reported whether it can resist THP-induced cardiotoxicity. The aim of this study was to investigate the effect of SchB on THP cardiotoxicity and its mechanism.Methods: The rat model of cardiotoxicity induced by THP was established, and SchB treatment was performed at the same time. The changes of ECG, cardiac coefficient, and echocardiogram were observed. The changes of myocardial tissue morphology were observed by H&E staining. Apoptosis was detected by TUNEL. The levels of LDH, BNP, CK-MB, cTnT, SOD, and MDA in serum were measured to observe the heart damage and oxidative stress state of rats. The expression of cleaved-caspase 9, pro/cleaved-caspase 3, Bcl-2/Bax, and cytosol and mitochondrial Cyt C and Bax was evaluated by western blot. H9c2 cardiomyocytes were cocultured with THP, SchB, and mPTP inhibitor CsA to detect the production of ROS and verify the above signaling pathways. The opening of mPTP and mitochondrial swelling were detected by mPTP kit and purified mitochondrial swelling kit.Results: After 8 weeks, a series of cardiotoxicity manifestations were observed in THP rats. These adverse effects can be effectively alleviated by SchB treatment. Further studies showed that SchB had strong antioxidant and antiapoptotic abilities in THP cardiotoxicity.Conclusion: SchB has an obvious protective effect on THP-induced cardiotoxicity. The mechanism may be closely related to the protection of mitochondrial function, inhibition of mPTP opening, and alleviation of oxidative stress and apoptosis of cardiomyocytes.

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