Naringenin ameliorates renal and platelet purinergic signalling alterations in high-cholesterol fed rats through the suppression of ROS and NF-κB signaling pathways

2016 ◽  
Vol 7 (1) ◽  
pp. 183-193 ◽  
Author(s):  
Yassine Chtourou ◽  
Zeineb Kamoun ◽  
Wissem Zarrouk ◽  
Mohammed Kebieche ◽  
Choumous Kallel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
Mitochondrial Dysfunction ◽  
Renal Tissue ◽  
Purinergic Signalling ◽  
High Cholesterol ◽  
Cholesterol Levels ◽  
Flavonoid Aglycone ◽  
And Oxidative Stress

The in vivo protective effect of Naringenin (NGEN), a natural flavonoid aglycone of naringin, against the mitochondrial dysfunction and oxidative stress induced by high cholesterol levels in the renal tissue.

scholarly journals Centella asiatica Attenuates Mitochondrial Dysfunction and Oxidative Stress in Aβ-Exposed Hippocampal Neurons

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Nora E. Gray ◽  
Jonathan A. Zweig ◽  
Donald G. Matthews ◽  
Maya Caruso ◽  
Joseph F. Quinn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Hippocampal Neurons ◽  
Neuroblastoma Cells ◽  
Water Extract ◽  
Centella Asiatica ◽  
Antioxidant Response ◽  
And Oxidative Stress

Centella asiatica has been used for centuries to enhance memory. We have previously shown that a water extract of Centella asiatica (CAW) protects against the deleterious effects of amyloid-β (Aβ) in neuroblastoma cells and attenuates Aβ-induced cognitive deficits in mice. Yet, the neuroprotective mechanism of CAW has yet to be thoroughly explored in neurons from these animals. This study investigates the effects of CAW on neuronal metabolism and oxidative stress in isolated Aβ-expressing neurons. Hippocampal neurons from amyloid precursor protein overexpressing Tg2576 mice and wild-type (WT) littermates were treated with CAW. In both genotypes, CAW increased the expression of antioxidant response genes which attenuated the Aβ-induced elevations in reactive oxygen species (ROS) and lipid peroxidation in Tg2576 neurons. CAW also improved mitochondrial function in both genotypes and increased the expression of electron transport chain enzymes and mitochondrial labeling, suggesting an increase in mitochondrial content. These data show that CAW protects against mitochondrial dysfunction and oxidative stress in Aβ-exposed hippocampal neurons which could contribute to the beneficial effects of the extract observed in vivo. Since CAW also improved mitochondrial function in the absence of Aβ, these results suggest a broader utility for other conditions where neuronal mitochondrial dysfunction occurs.

scholarly journals Aldosterone Excess Induced Mitochondria Decrease and Dysfunction via Mineralocorticoid Receptor and Oxidative Stress In Vitro and In Vivo

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 946
Author(s):  
Cheng-Hsuan Tsai ◽  
Chien-Ting Pan ◽  
Yi-Yao Chang ◽  
Shih-Yuan Peng ◽  
Po-Chin Lee ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dna ◽  
Mitochondrial Dysfunction ◽  
Mineralocorticoid Receptor ◽  
Cardiac Mitochondria ◽  
Mice Model ◽  
Atp Production ◽  
And Oxidative Stress

Aldosterone excess plays a major role in the progression of cardiac dysfunction and remodeling in clinical diseases such as primary aldosteronism and heart failure. However, the effect of aldosterone excess on cardiac mitochondria is unclear. In this study, we investigated the effect of aldosterone excess on cardiac mitochondrial dysfunction and its mechanisms in vitro and in vivo. We used H9c2 cardiomyocytes to investigate the effect and mechanism of aldosterone excess on cardiac mitochondria, and further investigated them in an aldosterone-infused ICR mice model. The results of the cell study showed that aldosterone excess decreased mitochondrial DNA, COX IV and SOD2 protein expressions, and mitochondria ATP production. These effects were abolished or attenuated by treatment with a mineralocorticoid receptor (MR) antagonist and antioxidant. With regard to the signal transduction pathway, aldosterone suppressed cardiac mitochondria through an MR/MAPK/p38/reactive oxygen species pathway. In the mouse model, aldosterone infusion decreased the amount of cardiac mitochondrial DNA and COX IV protein, and the effects were also attenuated by treatment with an MR antagonist and antioxidant. In conclusion, aldosterone excess induced a decrease in mitochondria and mitochondrial dysfunction via MRs and oxidative stress in vitro and in vivo.

Protective effect of tomato against N-methyl-N′-nitro-N-nitrosoguanidine–induced in vivo clastogenicity and oxidative stress

Nutrition ◽  
2004 ◽  
Vol 20 (9) ◽  
pp. 812-816 ◽  
Author(s):  
Balaiya Velmurugan ◽  
Vaidhyanathan Bhuvaneswari ◽  
Suresh K. Abraham ◽  
Siddavaram Nagini
Keyword(s):  
Oxidative Stress ◽  
Protective Effect ◽  
And Oxidative Stress

miR-187 Modulates Cardiomyocyte Apoptosis and Oxidative Stress in Myocardial Infarction Mice via Negatively Regulating DYRK2

2021 ◽  
Author(s):  
Fen Zhu ◽  
Zhili Yu ◽  
Dongsheng Li
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Protective Effect ◽  
Ischemia Reperfusion ◽  
Annexin V ◽  
Cardiomyocyte Apoptosis ◽  
Ros Generation ◽  
And Oxidative Stress

Abstract Background: Myocardial infarction is a serious representation of cardiovescular disease, however, ischemia–reperfusion (I/R) injury is an unpredictable complication of cardiovascular surgeries.Methods: MiR-187 or DYRK2 was inhibited or overexpressed in cardiomyocytes H/R models by pretreatment with miR-187 mimic or inhibitor or DYRK2 inhibitor to confirm the function of miR-187 in H/R. A myocardium I/R mouse model was established using miR-187 transgenic mice. Circulating levels of miR-187 or DYRK2 was detected by quantitative realtime PCR and protein expression was detected by western blotting. The cell viability in all groups was determined by MTT assay and the apoptosis ratio was detected by flow cytometry after staining with Annexin V-FITC. The effect of miR-187 on cellular ROS generation was examined by DCFH-DA. The level of lipid peroxidation and SOD expression were determined by MDA and SOD assay. Results: The findings indicated that miR-187 may be a possible regulator in the protective effect of H/R-induced cardiomyocyte apoptosis, cellular oxidative stress and leaded to DYRK2 suppression at a posttranscriptional level. Moreover, the improvement of miR-187 on H/R-induced cardiomyocyte injury contributed to the obstruction of DYRK2 expression. In addition, these results identified DYRK2 as the functional downstream target of miR-187 regulated myocardial infarction and oxidative stress. Conclusions: These present work provided the first insight into the function of miR-187 in successfully protect cardiomyocyte both in vivo and in vitro, and such a protective effect were mediated through the regulation of DYRK2 expression. Trial registration: Not Applicable.

scholarly journals Autophagy mitigates ethanol-induced mitochondrial dysfunction and oxidative stress in esophageal keratinocytes

PLoS ONE ◽  
2020 ◽  
Vol 15 (9) ◽  
pp. e0239625
Author(s):  
Prasanna M. Chandramouleeswaran ◽  
Manti Guha ◽  
Masataka Shimonosono ◽  
Kelly A. Whelan ◽  
Hisatsugu Maekawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
And Oxidative Stress
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