Read by QxMD icon Read

Hyperglycemia and H9C2

Yao-Te Huang, Chung-Hung Liu, Yao-Chih Yang, Ritu Aneja, Su-Ying Wen, Chih-Yang Huang, Wei-Wen Kuo
The prevalence of chronic hyperglycemia and its complications, imposing a critical burden on the worldwide economy and the global healthcare system, is a pressing issue. Mounting evidence indicates that oxidative stress and hypoxia, two noticeable features of hyperglycemia, play a joint crucial role in mediating cellular apoptosis. However, the underlying detailed molecular mechanism remains elusive. Triggered by the observation that insulin-like growth factor (IGF1)-binding protein 3 (IGFBP3) can mediate, in renal cells, high-glucose-induced apoptosis by elevating oxidative stress, we wish to, in this study, know whether or not the similar scenario holds in cardiac cells and, if so, to find its relevant molecular key players, thereby dissecting the underlying molecular pathway...
January 19, 2019: Journal of Cellular Physiology
Ravichandra Shivalingappa Davargaon, Asha Devi Sambe, Subramanyam Muthangi V V
Oxidative stress (OS) has been implicated in a variety of pathological conditions, including diabetes mellitus, characterized by hyperglycemia. In the present study, OS induced by hyperglycemia and the effect of trolox, a vitamin E analog, were studied in cardiomyocytes and H9c2 cells exposed to 15 to 33 mM glucose (HG) for 24 to 72 hours in Dulbecco modified Eagle medium. Cells treated wirh 24 or 33 mM glucose for 24 hours or above showed decreased viability and adenosine triphosphate (ATP) content with a concomitant increase in radicals of oxygen species, calcium (Ca2+ ), mitochondrial permeability transition, and oxidative markers, confirming that the cells were under stress...
December 4, 2018: Journal of Biochemical and Molecular Toxicology
Jing Liu, Yanming Li, Yi Tang, Jinghua Cheng, Jing Wang, Jianhua Li, Xiaohua Ma, Wei Zhuang, Jianbin Gong, Zhihong Liu
BACKGROUND: Rhein, an anthraquinone compound isolated from rhubarb, has been shown to protect the pancreatic β cells from hyperglycemia induced apoptosis in our previous studies. PURPOSE: In the present study, we examined whether rhein can protect myocardial cells against ischemia reperfusion (I/R)-induced apoptosis and investigated the underlying mechanism. METHODS: We used an in vitro model of myocardial hypoxia/reoxygenation (H/R) injury...
December 1, 2018: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
Jing Tian, Wenzhu Tang, Ming Xu, Chen Zhang, Pei Zhao, Tongtong Cao, Xiaoli Shan, Rong Lu, Wei Guo
BACKGROUND/AIMS: Shengmai San (SMS), prepared from Panax ginseng, Ophiopogon japonicus, and Schisandra chinensisin, has been widely used to treat ischemic disease. In this study, we investigated whether SMS may exert a beneficial effect in diabetic cardiomyopathy through improvement of mitochondrial lipid metabolism. METHODS: A leptin receptor-deficient db/db mouse model was utilized, and lean age-matched C57BLKS mice served as non-diabetic controls. Glucose and lipid profiles, myocardial structure, dimension, and function, and heart weight to tibial length ratio were determined...
2018: Cellular Physiology and Biochemistry
Rajvir Singh, Pedro Moreno, Roger J Hajjar, Djamel Lebeche
The adipokine resistin has been proposed to link obesity, insulin resistance and diabetes. We have previously reported that diabetic hearts express high levels of resistin while overexpression of resistin in adult rat hearts gives rise to a phenotype resembling diabetic cardiomyopathy. The transcriptional regulation of resistin in diabetic cardiac tissue is currently unknown. This study investigated the mechanism of resistin upregulation and the role of Serca2a in its transcriptional suppression. We demonstrate that restoration of Ca2+ homeostasis in diabetic hearts, through normalization of Serca2a function genetically and pharmacologically, suppressed resistin expression via inhibition of NFATc...
October 23, 2018: Scientific Reports
Weijian Hang, Benhong He, Jiehui Chen, Liangtao Xia, Bing Wen, Tao Liang, Xu Wang, Qianying Zhang, Yue Wu, Qingjie Chen, Juan Chen
Background: Type II diabetes (T2D)-induced cardiomyocyte hypertrophy is closely linked to the impairment of mitochondrial function. Berberine has been shown to be a promising effect for hypoglycemia in T2D models. High glucose-induced cardiomyocyte hypertrophy in vitro has been reported. The present study investigated the protective effect and the underlying mechanism of berberine on high glucose-induced H9C2 cell line. Methods: High glucose-induced H9C2 cell line was used to mimic the hyperglycemia resulting in cardiomyocyte hypertrophy...
2018: Frontiers in Pharmacology
Chen Zhao, Qile Shen
Hyperglycemia may induce diabetic cardiomyopathy (DC). In the current study, the mechanism underlying the alleviation of high glucose (HG)‑induced impairments in the proliferation of H9c2 embryo cardiomyocyte proliferation by small ubiquitin‑like modifier 2 (SUMO2) overexpression was investigated. H9c2 cell morphology was identified as classical long shuttle type by optical microscopy. The viability of HG‑injured H9c2 cells was evaluated by a Cell Counting Kit‑8 assay and the results indicated that viability was inhibited in a dose‑dependent (5...
December 2018: Molecular Medicine Reports
Nair Anupama, M R Preetha Rani, G L Shyni, K G Raghu
Several mechanisms have been proposed for the heart dysfunction during hyperglycemia. The aim of the present in vitro study is to elucidate the role of alterations in redox homeostasis in the induction of apoptosis during hyperglycemia in H9c2 cells via dysfunction in mitochondria and polyol pathway and evaluation of the beneficial effect of cinnamic acid against the same. The H9c2 cells were incubated with 33 mM glucose for 48 h to simulate the diabetic condition. Cell injury was confirmed with a significant increase of atrial natriuretic peptide and lactate dehydrogenase release...
December 2018: Toxicology in Vitro: An International Journal Published in Association with BIBRA
Kai-Chun Cheng, Wei-Ting Chang, Yingxiao Li, Yung-Ze Cheng, Juei-Tang Cheng, Zhih-Cherng Chen
Peroxisome proliferator-activated receptor δ (PPARδ), the predominant PPAR subtype in the heart, is known to regulate cardiac function. PPARδ activation may inhibit cardiac hypertrophy in H9c2 cells while the potential mechanism has not been elucidated. Then, H9c2 cells incubated with high glucose to induce hypertrophy were used to investigate using GW0742 to activate PPARδ. The fluorescence assays were applied to determine the changes in cell size, cellular calcium levels, and free radicals. Western blot analyses for hypertrophic signals and assays of messenger RNA (mRNA) levels for hypertrophic biomarkers were performed...
November 2018: Journal of Cellular Biochemistry
Maria Consiglia Trotta, Monica Salerno, Anna Lisa Brigida, Vincenzo Monda, Antonietta Messina, Carmela Fiore, Roberto Avola, Renato Bernardini, Francesco Sessa, Gabriella Marsala, Guido N Zanghì, Giovanni Messina, Michele D'Amico, Clara Di Filippo
Long QT syndrome (LQTS) is characterized by prolonged QT interval, leading to sudden cardiac death. Hyperglycemia is an important risk factor for LQTS, inhibiting the cardiac rapid component delayed rectifier K+ current (Iks), responsible for QT interval. We previously showed that the new ALR2 inhibitor BF-5m supplies cardioprotection from QT prolongation induced by high glucose concentration in the medium, reducing QT interval prolongation and preserving morphology. Here we investigated the effects of BF-5m on cell cytotoxicity and viability in H9c2 cells, and on cellular potassium ion channels expression...
April 3, 2018: Oncotarget
M R Preetha Rani, Nair Anupama, Mohan Sreelekshmi, K G Raghu
A series of cardiovascular complications associated with hyperglycemia is a critical threat to the diabetic population. Here we elucidate the link between hyperglycemia and cardiovascular diseases onset, focusing on oxidative stress and associated cardiac dysfunctions. The contribution of advanced glycation end products (AGE) and protein kinase C (PKC) signaling is extensively studied. For induction of hyperglycemia, H9c2 cells were incubated with 33 mM glucose for 48 h to simulate the diabetic condition in in vitro system...
April 2018: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
Xuemei Chen, Jianchang Qian, Lintao Wang, Jieli Li, Yunjie Zhao, Jibo Han, Zia Khan, Xiaojun Chen, Jingying Wang, Guang Liang
PURPOSE: Suppression of inflammation and oxidative stress is an attractive strategy to against diabetic cardiomyopathy (DCM). Kaempferol (KPF) exerts both anti-inflammatory and antioxidant pharmacological properties. However, little is known about the effect of KPF on protecting myocardial injury in diabetes. The present study aimed to investigate the effect of KPF on DCM and underlying mechanism. METHODS: Anti-inflammation and anti-oxidative stress activities of KPF were evaluated in H9c2 cells or primary cardiomyocytes by real-time quantitate PCR, immunoblotting, immunofluorescence, ELISA, and FACS...
April 2018: Endocrine
Fan Deng, Shuang Wang, Liangqing Zhang, Xiang Xie, Shuyun Cai, Haobo Li, Gui-Ling Xie, Hui-Lai Miao, Changmin Yang, Xin Liu, Zhengyuan Xia
BACKGROUND/AIMS: Hearts from diabetic subjects are susceptible to myocardial ischemia reperfusion (I/R) injury. Propofol has been shown to protect against myocardial I/R injury due to its antioxidant properties while the underlying mechanism remained incompletely understood. Thus, this study aimed to determine whether or not propofol could attenuate myocardial I/R injury by attenuating mitochondrial dysfunction/damage through upregulating Caveolin (Cav)-3 under hyperglycemia. METHODS: Cultured rat cardiomyocyte H9C2 cells were subjected to hypoxia/reoxygenation (H/R) in the absence or presence of propofol under high glucose (HG), and cell viability, lactate dehydrogenase (LDH) and mitochondrial viability as well as creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) and intracellular adenosine triphosphate (ATP) content were measured with colorimetric Enzyme-Linked Immunosorbent Assays...
2017: Cellular Physiology and Biochemistry
Min Liu, Songhe Lu, Wei He, Le Zhang, Ying Ma, Ping Lv, Meijuan Ma, Wenjun Yu, Jiaxing Wang, Mingming Zhang, Yingmei Zhang, Yan Li
Mitochondrial aldehyde dehydrogenase 2 (ALDH2), an important enzyme in the elimination of toxic aldehydes, is involved in cardioprotection against diabetes mellitus. This study was designed to examine the mechanism behind ALDH2-offered protection against high glucose exposure with a focus on autophagy. H9C2 cells were cultured with normal or high glucose medium in the presence or absence of the ALDH2 agonist Alda-1. GFP-LC3 puncta and immunofluorescence were employed to assess autophagosome formation. Western blotting was applied to evaluate autophagy protein markers Atg5, LC3, p62, ULK1 phosphorylation and ALDH2...
February 2018: Toxicology Letters
Yu-Hsin Chiu, Po-Ming Ku, Yung-Ze Cheng, Yingxiao Li, Juei-Tang Cheng, Ho-Shan Niu
The signal transducer and activator of transcription 3 (STAT3) is known to be involved in hypertrophy and fibrosis in cardiac dysfunction. The activation of STAT3 via the phosphorylation of STAT3 is required for the production of functional activity. It has been established that lipopolysaccharide (LPS)‑induced phosphorylation of STAT3 in cardiomyocytes primarily occurs through a direct receptor‑mediated action. This effect is demonstrated to be produced rapidly. STAT3 in cardiac fibrosis of diabetes is induced by high glucose through promotion of the STAT3‑associated signaling pathway...
January 2018: Molecular Medicine Reports
Yue Guo, Xiaodong Zhuang, Zena Huang, Jing Zou, Daya Yang, Xun Hu, Zhimin Du, Lichun Wang, Xinxue Liao
Cardiac inflammation and oxidative stress play a key role in the pathogenesis of diabetic cardiomyopathy (DCM). The anti-aging protein Klotho has been found to protect cells from inflammation and oxidative stress. The current study aimed to explore the cardioprotective effects of Klotho on DCM and the underlying mechanisms. H9c2 cells and neonatal cardiomyocytes were incubated with 33mM glucose in the presence or absence of Klotho. Klotho pretreatment effectively inhibited high glucose-induced inflammation, ROS generation, apoptosis, mitochondrial dysfunction, fibrosis and hypertrophy in both H9c2 cells and neonatal cardiomyocytes...
January 2018: Biochimica et biophysica acta. Molecular basis of disease
Hong Li, Changqing Xu, Quanfeng Li, Xiuxiang Gao, Erkio Sugano, Hiroshi Tomita, Liming Yang, Sa Shi
Mitochondrial oxidative stress is thought to be a key contributor towards the development of diabetic cardiomyopathy. Thioredoxin 2 (Trx2) is a mitochondrial antioxidant that, along with Trx reductase 2 (TrxR2) and peroxiredoxin 3 (Prx3), scavenges H₂O₂ and offers protection against oxidative stress. Our previous study showed that TrxR inhibitors resulted in Trx2 oxidation and increased ROS emission from mitochondria. In the present study, we observed that TrxR inhibition also impaired the contractile function of isolated heart...
September 15, 2017: International Journal of Molecular Sciences
Guang-Yu Wang, Ya-Guang Bi, Xiang-Dong Liu, Yu Zhao, Jun-Feng Han, Meng Wei, Qing-Yong Zhang
Background: Increased cardiomyocyte apoptosis under high glucose condition contributes to diabetic cardiomyopathy. Degradation of cardiac Connexin43 (Cx43) has been associated with cardiac dysfunction in diabetic heart. Clinical and experimental studies suggested that metformin (Met) exhibits cardioprotective properties against diabetes. Aim: The aim of this study was to investigate the effect and underlying signaling mechanisms of metformin on apoptosis and Cx43 expression in H9c2 cells presenting with hyperglycemia conditions...
2017: International Journal of Medical Sciences
Bin Zhou, Yan Leng, Shao-Qing Lei, Zhong-Yuan Xia
Although the mechanism remains unclear, ischemic post‑conditioning (IPO) is a promising approach to combat myocardial ischemia reperfusion (IR) injury; however, it has been proven ineffective in diabetes. The present study aimed to identify whether hyperglycemia‑induced AMP‑activated protein kinase (AMPK) inhibition contributes to the ineffectiveness of IPO via autophagy attenuation in diabetic hearts. Diabetic and non‑diabetic rats were subjected to myocardial IR and/or IPO with/without treatment with the AMPK activator A‑769662 and/or autophagy inhibitor 3‑methyladenine (3‑MA)...
September 2017: Molecular Medicine Reports
Guang-Yu Wang, Ya-Guang Bi, Xiang-Dong Liu, Jun-Feng Han, Meng Wei, Qing-Yong Zhang
The expression of connexin43 (Cx43) protein and the apoptotic rate of cardiomyocytes may be regulated by autophagy and associated with diabetic cardiomyopathy. It is possible that the beneficial effect of resveratrol on diabetic cardiomyocytes occurs via the autophagy pathway. However, it remains to be elucidated whether resveratrol treatment may attenuate the hyperglycemia‑induced remodeling of Cx43 and apoptosis through the regulation of autophagy. H9c2 cardiac cells were incubated with 5.5 and 25 mM glucose, 25 mM glucose with chloroquine (50 µM), and 25 mM glucose with or without resveratrol (10, 25 µM) for 24 h...
September 2017: Molecular Medicine Reports
Fetch more papers »
Fetching more papers... Fetching...
Read by QxMD. Sign in or create an account to discover new knowledge that matter to you.
Remove bar
Read by QxMD icon Read

Search Tips

Use Boolean operators: AND/OR

diabetic AND foot
diabetes OR diabetic

Exclude a word using the 'minus' sign

Virchow -triad

Use Parentheses

water AND (cup OR glass)

Add an asterisk (*) at end of a word to include word stems

Neuro* will search for Neurology, Neuroscientist, Neurological, and so on

Use quotes to search for an exact phrase

"primary prevention of cancer"
(heart or cardiac or cardio*) AND arrest -"American Heart Association"