scholarly journals Tauroursodeoxycholic Acid Alleviates H2O2-Induced Oxidative Stress and Apoptosis via Suppressing Endoplasmic Reticulum Stress in Neonatal Rat Cardiomyocytes

Dose-Response ◽  
2018 ◽  
Vol 16 (3) ◽  
pp. 155932581878263 ◽  
Author(s):  
Lin Zhang ◽  
Yanmin Wang
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Reactive Oxygen Species Generation ◽  
Neonatal Rat ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Tauroursodeoxycholic Acid ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Introduction: We aimed to test the mechanism of protective effects of tauroursodeoxycholic acid (TUDCA) on cardiovascular disease using cultured cardiomyocytes. Methods: Neonatal rat cardiomyocytes (NRCMs) were isolated and cultured and then the cells were divided into 4 groups based on the treatments: control group (cells treated with culture medium), H2O2/thapsigargin (TG) group (cells treated with oxidative stress and endoplasmic reticulum [ER] stress inducer), TUDCA group, and H2O2/TG + TUDCA group. The treated NRCMs were then subjected to serial analyses including flow cytometry, enzyme-linked immunosorbent assay, and Western blotting. Results: Tauroursodeoxycholic acid significantly attenuated H2O2-induced reactive oxygen species generation and lactate dehydrogenase release and restored H2O2-induced reductions of glutathione and superoxide dismutase levels in NRCMs. Tauroursodeoxycholic acid also alleviated H2O2-induced cardiomyocytes apoptosis, as well as the Bax/Bcl2 ratio compared with that of H2O2 treated alone. In addition, TUDCA suppressed TG-induced ER stress as reflected by inversing cell viability and the expression levels of glucose-regulated protein 78 kDa and C/enhancer-binding protein homologous protein. Conclusion: Our data indicated that TUDCA-mediated inhibition on H2O2-induced oxidative stress and cardiomyocytes apoptosis was through suppressing ER stress, and TUDCA possesses the potential to be developed as therapeutic tool in clinical use for cardiovascular diseases.

scholarly journals Crosstalk between endoplasmic reticulum stress and oxidative stress: a dynamic duo in multiple myeloma

2021 ◽  
Author(s):  
Sinan Xiong ◽  
Wee-Joo Chng ◽  
Jianbiao Zhou
Keyword(s):  
Oxidative Stress ◽  
Multiple Myeloma ◽  
Endoplasmic Reticulum ◽  
Er Stress ◽  
Cell Fate ◽  
Stress Responses ◽  
Plasma Cells ◽  
Reactive Oxygen Species Generation ◽  
Future Research ◽  
And Oxidative Stress

AbstractUnder physiological and pathological conditions, cells activate the unfolded protein response (UPR) to deal with the accumulation of unfolded or misfolded proteins in the endoplasmic reticulum. Multiple myeloma (MM) is a hematological malignancy arising from immunoglobulin-secreting plasma cells. MM cells are subject to continual ER stress and highly dependent on the UPR signaling activation due to overproduction of paraproteins. Mounting evidence suggests the close linkage between ER stress and oxidative stress, demonstrated by overlapping signaling pathways and inter-organelle communication pivotal to cell fate decision. Imbalance of intracellular homeostasis can lead to deranged control of cellular functions and engage apoptosis due to mutual activation between ER stress and reactive oxygen species generation through a self-perpetuating cycle. Here, we present accumulating evidence showing the interactive roles of redox homeostasis and proteostasis in MM pathogenesis and drug resistance, which would be helpful in elucidating the still underdefined molecular pathways linking ER stress and oxidative stress in MM. Lastly, we highlight future research directions in the development of anti-myeloma therapy, focusing particularly on targeting redox signaling and ER stress responses.

Oxidative stress enhances phosphorylation of p53 in neonatal rat cardiomyocytes

2007 ◽  
Vol 303 (1-2) ◽  
pp. 167-174 ◽  
Author(s):  
Xilin Long ◽  
Michael J. Goldenthal ◽  
José Marín-García
Keyword(s):  
Oxidative Stress ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Propofol attenuates H2O2-induced oxidative stress and apoptosis via the mitochondria- and ER-medicated pathways in neonatal rat cardiomyocytes

APOPTOSIS ◽  
2017 ◽  
Vol 22 (5) ◽  
pp. 639-646 ◽  
Author(s):  
Xue-Ru Liu ◽  
Lu Cao ◽  
Tao Li ◽  
Lin-Lin Chen ◽  
Yi-Yan Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Selenium deficiency aggravates T-2 toxin-induced injury of primary neonatal rat cardiomyocytes through ER stress

2018 ◽  
Vol 285 ◽  
pp. 96-105 ◽  
Author(s):  
Jing Xu ◽  
Shengchi Pan ◽  
Fang Gan ◽  
Shu Hao ◽  
Dandan Liu ◽  
...  
Keyword(s):  
Er Stress ◽  
Selenium Deficiency ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Abstract 72: Hydrogen Sulfide Prevents Myocardial Hypertrophy in a Klf5-dependent Manner

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Guoliang Meng ◽  
Liping Xie ◽  
Yong Ji
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Promoter Activity ◽  
Myocardial Hypertrophy ◽  
Neonatal Rat ◽  
Cardiomyocyte Hypertrophy ◽  
Dependent Manner ◽  
Ang Ii ◽  
Rat Cardiomyocytes ◽  
Neonatal Rat Cardiomyocytes

Rationale: H 2 S is a gasotransmitter that regulates multiple cardiovascular functions. Krüppel-like transcription factor (KLF) exerts diverse functions in the cardiovascular system. Objectives: The aim of present study was to investigate the effect of hydrogen sulfide (H 2 S) on myocardial hypertrophy. Methods and results: Myocardial samples of 22 patients with left ventricle hypertrophy were collected and underwent histological and molecular biological analysis. Spontaneously hypertensive rats (SHR) and neonatal rat cardiomyocytes were studied for functional and signaling response to GYY4137, a H 2 S-releasing compound. Expression of cystathionine -lyase (CSE), a main enzyme for H 2 S generation in human heart, decreased in human hypertrophic myocardium, while KLF5 expression increased. In SHR treated with GYY4137 for 4 weeks, myocardial hypertrophy was inhibited as evidenced by improvement in cardiac structural parameters, heart mass index, size of cardiac myocytes and expression of atrial natriuretic peptide (ANP). Levels of oxidative stress and phosphorylation of mitogen-activated protein kinases were also decreased after H 2 S treatment. H 2 S diminished expression of the KLF5 in myocardium of SHR and in neonatal rat cardiomyocytes rendered hypertrophy by angiotensin II (Ang II). H 2 S also inhibited ANP promoter activity and ANP expression in Ang II-induced neonatal rat cardiomyocyte hypertrophy, and these effects were suppressed by KLF5 knockdown. KLF5 promoter activity was increased by Ang II stimulation, and this was reversed by H 2 S. H 2 S also decreased activity of specificity protein-1 (SP-1) binding to the KLF5 promoter and attenuated KLF5 nuclear translocation by Ang II stimulation. Conclusion: H 2 S attenuated myocardial hypertrophy, which might be related to inhibiting oxidative stress and decreasing ANP transcription activity in a KLF5-dependent manner.

scholarly journals Ononin Alleviates Doxorubicin-Induced Cardiotoxicity by Inhibiting ER Stress Through Activation of SIRT3

2021 ◽  
Author(s):  
Shimin Sun ◽  
Jingfan Weng ◽  
Qi Yang ◽  
Xingxiao Huang ◽  
Hanlin Zhang ◽  
...  
Keyword(s):  
Er Stress ◽  
Myocardial Injury ◽  
Molecular Mechanisms ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Rat Cardiomyocytes

Abstract Introduction Doxorubicin (DOX) is a powerful anthracycline antineoplastic drug, but the clinical application of DOX is seriously limited by its dose-dependent cardiotoxicity. Ononin is a natural isoflavone glycoside and plays a key role in modulating apoptosis related signaling pathways. The aim of this study was to assess the possible cardioprotective effects of Ononin in DOX-induced cardiotoxicity and the underlying molecular mechanisms. Materials and methods Wistar rats were treated with normal saline, DOX with or without Ononin. After the last administration, cardiac function was evaluated by echocardiography. Rats were then sacrificed for histological and TUNEL analyses, with immunological detection for β-actinin, Bax, Bcl-2, GRP78, CHOP and SIRT3. An enzyme-linked immunosorbent assay was performed to assess the myocardial injury markers. H9C2 cells were treated with vehicle, DOX with or without Ononin. Then, 3-TYP was used to find out the relationship between ER stress and SIRT3. Results Ononin treatment ameliorated DOX-induced myocardial injury as demonstrated by echocardiography. Ononin partially restored DOX-induced cardiac dysfunction, both LVEF and LVFS were increased under the cotreatment of Ononin. Ononin also inhibited DOX-induced ER stress and apoptosis in rat cardiomyocytes and H9C2 cells. DOX group had a higher Bax/Bcl-2 ratio, GRP78 and CHOP expression then control group, but Ononin treatment improved these results. This effect was associated with SIRT3 activity, moreover, selective inhibition of SIRT3 blocked the protective effects of Ononin. Conclusion In the present study, we tested the hypothesis that Ononin may protect against DOX-induced cardiomyopathy through ER stress both in vitro and in vivo. Ononin is able to protect against DOX-induced cardiotoxicity by inhibiting ER stress and apoptosis, this effect may via stimulation of the SIRT3 pathway.

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