scholarly journals Dexmedetomidine attenuates H2O2-induced apoptosis of rat cardiomyocytes independently of antioxidant enzyme expression

2021 ◽  
Author(s):  
Xiaojian Weng ◽  
Wenjiao Shi ◽  
Xiaodan Zhang ◽  
Jianer Du
Keyword(s):  
Antioxidant Enzyme ◽  
Enzyme Expression ◽  
Rat Cardiomyocytes ◽  
Induced Apoptosis

Effect of phorbol ester (PMA) on antioxidant enzyme expression in TGF-β1-induced apoptosis in primary cultures of hepatocytes

BioFactors ◽  
1998 ◽  
Vol 8 (1-2) ◽  
pp. 65-71 ◽  
Author(s):  
Carmen Díez-Fernández ◽  
Nuria Sanz ◽  
Armin Wolf ◽  
María Cascales
Keyword(s):  
Antioxidant Enzyme ◽  
Phorbol Ester ◽  
Primary Cultures ◽  
Enzyme Expression ◽  
Induced Apoptosis ◽  
Tgf Β1

Hexarelin protects rat cardiomyocytes from angiotensin II-induced apoptosis in vitro

2004 ◽  
Vol 286 (3) ◽  
pp. H1063-H1069 ◽  
Author(s):  
Jin-Jiang Pang ◽  
Rong-Kun Xu ◽  
Xiang-Bin Xu ◽  
Ji-Min Cao ◽  
Chao Ni ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Caspase 3 ◽  
Cardiomyocyte Apoptosis ◽  
Protective Effects ◽  
Ang Ii ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Rat Cardiomyocytes ◽  
Induced Apoptosis

Loss of cardiomyocytes by apoptosis is proposed to cause heart failure. Angiotensin II (ANG II), an important neurohormonal factor during heart failure, can induce cardiomyocyte apoptosis. Inasmuch as hexarelin has been reported to have protective effects in this process, we examined whether hexarelin can prevent cardiomyocytes from ANG II-induced cell death. Cultured cardiomyocytes from neonatal rats were stimulated with ANG II. Apoptosis was evaluated using fluorescence microscopy, TdT-mediated dUTP nick-end labeling (TUNEL) method, flow cytometry, DNA laddering, and analysis of cell viability by (3,4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT). It was found that incubation with 0.1 μmol/l ANG II for 48 h increased cardiomyocyte apoptosis. Administration of 0.1 μmol/l hexarelin significantly decreased this ANG II-induced apoptosis and DNA fragmentation and increased myocyte viability. To further investigate the underlying mechanisms, caspase-3 activity assay and mRNA expression of Bax, Bcl-2, and growth hormone secretagogue receptor (GHS-R; the supposed hexarelin binding site) were examined. GHS-R mRNA was abundantly expressed in cardiomyocytes and was upregulated after administration of hexarelin. These results suggest that hexarelin abates cardiomyocytes from ANG II-induced apoptosis possibly via inhibiting the increased caspase-3 activity and Bax expression induced by ANG II and by increasing the expression of Bcl-2, which is depressed by ANG II. Whether the upregulated expression of GHS-R induced by hexarelin is associated with this antiapoptotic effect deserves further investigation.

scholarly journals Tobacco and Antiretrovirals Modulate Transporter, Metabolic Enzyme, and Antioxidant Enzyme Expression and Function in Polarized Macrophages

2019 ◽  
Vol 16 (5) ◽  
pp. 354-363 ◽  
Author(s):  
Ying Mu ◽  
Benjamin J. Patters ◽  
Narasimha M. Midde ◽  
Hui He ◽  
Santosh Kumar ◽  
...  
Keyword(s):  
Antioxidant Enzyme ◽  
Metabolic Enzyme ◽  
Enzyme Expression ◽  
And Function

scholarly journals Resistance Exercise And Doxorubicin Treatment: Effects On Antioxidant Enzyme Expression In Type Ii Muscle

2019 ◽  
Vol 51 (Supplement) ◽  
pp. 500
Author(s):  
Salaheddin Sharif ◽  
David S. Hydock ◽  
Kelsey A. Daehlin ◽  
Mackenzie D. Twaddle ◽  
Allison T. Tigner ◽  
...  
Keyword(s):  
Resistance Exercise ◽  
Antioxidant Enzyme ◽  
Treatment Effects ◽  
Type Ii ◽  
Enzyme Expression ◽  
Doxorubicin Treatment

Nitric oxide signaling in stretch‐induced apoptosis of neonatal rat cardiomyocytes

2006 ◽  
Vol 20 (11) ◽  
pp. 1883-1885 ◽  
Author(s):  
Xudong Liao ◽  
Jun‐Ming Liu ◽  
Lei Du ◽  
Aihui Tang ◽  
Yingli Shang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Neonatal Rat ◽  
Rat Cardiomyocytes ◽  
Nitric Oxide Signaling ◽  
Neonatal Rat Cardiomyocytes ◽  
Induced Apoptosis

scholarly journals 3,3′-Diindolylmethane Promotes BDNF and Antioxidant Enzyme Formation via TrkB/Akt Pathway Activation for Neuroprotection against Oxidative Stress-Induced Apoptosis in Hippocampal Neuronal Cells

Antioxidants ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 3 ◽  
Author(s):  
Bo Dam Lee ◽  
Jae-Myung Yoo ◽  
Seong Yeon Baek ◽  
Fu Yi Li ◽  
Dai-Eun Sok ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Neurodegenerative Diseases ◽  
Antioxidant Enzyme ◽  
Neuronal Cells ◽  
Akt Pathway ◽  
Heme Oxygenase 1 ◽  
Enzyme Formation ◽  
Induced Apoptosis

3,3′-Diindolylmethane (DIM), a metabolite of indole-3-carbinol present in Brassicaceae vegetables, possesses various health-promoting effects. Nonetheless, the effect of DIM on neurodegenerative diseases has not been elucidated clearly. In this study, we hypothesized DIM may protect neuronal cells against oxidative stress-induced apoptosis by promoting the formation of brain-derived neurotrophic factor (BDNF) and antioxidant enzymes through stabilizing the activation of the tropomyosin-related kinase receptor B (TrkB) cascade and we investigated the effect of DIM on oxidative stress-mediated neurodegenerative models. DIM protected neuronal cells against oxidative stress-induced apoptosis by regulating the expression of apoptosis-related proteins in glutamate-treated HT-22 cells. Additionally, DIM improved the expression of BDNF and antioxidant enzymes, such as heme oxygenase-1, glutamate-cysteine ligase catalytic subunit, and NAD(P)H quinine oxidoreductase-1, by promoting the activation of the TrkB/protein kinase B (Akt) pathway in the cells. Consistent with in vitro studies, DIM attenuated memory impairment by protecting hippocampal neuronal cells against oxidative damage in scopolamine-treated mice. Conclusionally, DIM exerted neuroprotective and antioxidant actions through the activation of both BDNF production and antioxidant enzyme formation in accordance with the TrkB/Akt pathway in neuronal cells. Such an effect of DIM may provide information for the application of DIM in the prevention of and therapy for neurodegenerative diseases.

Severe oxidative damage in multiple sclerosis lesions coincides with enhanced antioxidant enzyme expression

2008 ◽  
Vol 45 (12) ◽  
pp. 1729-1737 ◽  
Author(s):  
J. van Horssen ◽  
G. Schreibelt ◽  
J. Drexhage ◽  
T. Hazes ◽  
C.D. Dijkstra ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Oxidative Damage ◽  
Antioxidant Enzyme ◽  
Enzyme Expression
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