Nitric Oxide/Reactive Oxygen Species Generation and Nitroso/Redox Imbalance in Heart Failure: From Molecular Mechanisms to Therapeutic Implications

2011 ◽  
Vol 14 (2) ◽  
pp. 289-331 ◽  
Author(s):  
Chiara Nediani ◽  
Laura Raimondi ◽  
Elisabetta Borchi ◽  
Elisabetta Cerbai
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Molecular Mechanisms ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Therapeutic Implications ◽  
Redox Imbalance

scholarly journals Metformin Protects H9C2 Cardiomyocytes from High-Glucose and Hypoxia/Reoxygenation Injury via Inhibition of Reactive Oxygen Species Generation and Inflammatory Responses: Role of AMPK and JNK

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Mingyan Hu ◽  
Ping Ye ◽  
Hua Liao ◽  
Manhua Chen ◽  
Feiyan Yang
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Viability ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Compound C ◽  
Hypoxia Reoxygenation

Metformin is a first-line drug for the management of type 2 diabetes. Recent studies suggested cardioprotective effects of metformin against ischemia/reperfusion injury. However, it remains elusive whether metformin provides direct protection against hypoxia/reoxygenation (H/R) injury in cardiomyocytes under normal or hyperglycemic conditions. This study in H9C2 rat cardiomyoblasts was designed to determine cell viability under H/R and high-glucose (HG, 33 mM) conditions and the effects of cotreatment with various concentrations of metformin (0, 1, 5, and 10 mM). We further elucidated molecular mechanisms underlying metformin-induced cytoprotection, especially the possible involvement of AMP-activated protein kinase (AMPK) and Jun NH(2)-terminal kinase (JNK). Results indicated that 5 mM metformin improved cell viability, mitochondrial integrity, and respiratory chain activity under HG and/or H/R (P<0.05). The beneficial effects were associated with reduced levels of reactive oxygen species generation and proinflammatory cytokines (TNF-α, IL-1α, and IL-6) (P<0.05). Metformin enhanced phosphorylation level of AMPK and suppressed HG + H/R induced JNK activation. Inhibitor of AMPK (compound C) or activator of JNK (anisomycin) abolished the cytoprotective effects of metformin. In conclusion, our study demonstrated for the first time that metformin possessed direct cytoprotective effects against HG and H/R injury in cardiac cells via signaling mechanisms involving activation of AMPK and concomitant inhibition of JNK.

scholarly journals Modulation of metabolic activity of phagocytes by antihistamines

2011 ◽  
Vol 4 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Antonin Lojek ◽  
Milan Číž ◽  
Michaela Pekarová ◽  
Gabriela Ambrožová ◽  
Ondřej Vašíček ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Metabolic Activity ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Inhibitory Effect ◽  
Oxygen Species ◽  
Antioxidative Properties ◽  
Enhanced Chemiluminescence ◽  
Inos Protein Expression

Modulation of metabolic activity of phagocytes by antihistaminesThe purpose of the study was to investigate the effects of H1-antihistamines of the 1stgeneration (antazoline, bromadryl, brompheniramine, dithiaden, cyclizine, chlorcyclizine, chlorpheniramine, clemastine) and the 2ndgeneration (acrivastine, ketotifen, and loratadine) on the respiratory burst of phagocytes. Reactive oxygen species generation in neutrophils isolated from rat blood was measured using luminol-enhanced chemiluminescence. Changes in nitrite formation and iNOS protein expression by RAW 264.7 macrophages were analysed using Griess reaction and Western blotting. The antioxidative properties of drugs in cell-free systems were detected spectrophotometrically, luminometrically, fluorimetrically, and amperometrically. The majority of the H1-antihistamines tested (bromadryl, brompheniramine, chlorcyclizine, chlorpheniramine, clemastine, dithiaden, and ketotifen) exhibited a significant inhibitory effect on the chemiluminescence activity of phagocytes. H1-antihistamines did not show significant scavenging properties against superoxide anion and hydroxyl radical, thus this could not contribute to the inhibition of chemiluminescence. H1-antihistamines had a different ability to modulate nitric oxide production by LPS-stimulated macrophages. Bromadryl, clemastine, and dithiaden were the most effective since they inhibited iNOS expression, which was followed by a significant reduction in nitrite levels. H1-antihistamines had no scavenging activity against nitric oxide. It can be concluded that the effects observed in the H1-antihistamines tested are not mediated exclusively via H1-receptor pathway or by direct antioxidative properties. Based on our results, antihistamines not interfering with the microbicidal mechanisms of leukocytes (antazoline, acrivastine and cyclizine) could be used preferentially in infections. Other antihistamines should be used, under pathological conditions accompanied by the overproduction of reactive oxygen species.

Regulatory mechanisms of nitric oxide and reactive oxygen species generation and their role in plant immunity

Nitric Oxide ◽  
2011 ◽  
Vol 25 (2) ◽  
pp. 216-221 ◽  
Author(s):  
Hirofumi Yoshioka ◽  
Keisuke Mase ◽  
Miki Yoshioka ◽  
Michie Kobayashi ◽  
Shuta Asai
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Plant Immunity ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Regulatory Mechanisms ◽  
Oxygen Species

scholarly journals The H2S Donor GYY4137 Stimulates Reactive Oxygen Species Generation in BV2 Cells While Suppressing the Secretion of TNF and Nitric Oxide

Molecules ◽  
2018 ◽  
Vol 23 (11) ◽  
pp. 2966 ◽  
Author(s):  
Milica Lazarević ◽  
Emanuela Mazzon ◽  
Miljana Momčilović ◽  
Maria Basile ◽  
Giuseppe Colletti ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Microglial Cells ◽  
Oxygen Species ◽  
Bv2 Cells ◽  
The Central Nervous System

GYY4137 is a hydrogen sulfide (H2S) donor that has been shown to act in an anti-inflammatory manner in vitro and in vivo. Microglial cells are among the major players in immunoinflammatory, degenerative, and neoplastic disorders of the central nervous system, including multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and glioblastoma multiforme. So far, the effects of GYY4137 on microglial cells have not been thoroughly investigated. In this study, BV2 microglial cells were stimulated with interferon-gamma and lipopolysaccharide and treated with GYY4137. The agent did not influence the viability of BV2 cells in concentrations up to 200 μM. It inhibited tumor necrosis factor but not interleukin-6 production. Expression of CD40 and CD86 were reduced under the influence of the donor. The phagocytic ability of BV2 cells and nitric oxide production were also affected by the agent. Surprisingly, GYY4137 upregulated generation of reactive oxygen species (ROS) by BV2 cells. The effect was mimicked by another H2S donor, Na2S, and it was not reproduced in macrophages. Our results demonstrate that GYY4137 downregulates inflammatory properties of BV2 cells but increases their ability to generate ROS. Further investigation of this unexpected phenomenon is warranted.

scholarly journals HUBUNGAN KADAR ASAM URAT DENGAN KEJADIAN GAGAL JANTUNG AKUT PADA PASIEN HIPERTENSI

e-CliniC ◽  
2015 ◽  
Vol 3 (1) ◽  
Author(s):  
Rezuanto Pualillin ◽  
Starry H. Rampengan ◽  
Frans Wantania
Keyword(s):  
Nitric Oxide ◽  
Heart Failure ◽  
Reactive Oxygen Species ◽  
Uric Acid ◽  
Acute Heart Failure ◽  
Heart Muscle ◽  
Odds Ratio ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Probability Sampling

Abstract: Long period of hypertension causes enlargement of the heart muscle, which leads to heart failure. Increased uric acid will causes endothelial dysfunction nas a result of the over production of reactive oxygen species (ROS), decrease the amount of nitric oxide (NO), increased rennin production, and the occurrence of inflammatory reactions. This speeds up the deterioration of the heart muscle, causing acute phase of heart failure. This study aimed to determine the relationship between uric acid levels and the incidence of acute heart failure in hypertensive patients in the emergency department and hypertension clinic of Prof. Dr R.D Kandou Hospital in Manado. This was an analytical observation by using the cross-sectional design. By using a non-probability sampling method we found 40 people as samples who had been diagnosed with heart failure due to hypertension. There were 15 samples that had experienced acute heart failure and 25 samples did not. Logistic Regression Test results stated that there was no significant effect of uric acid level with the incidence of acute heart failure (p = 0.188), with the value of the odds ratio of 1.198. Conclusion: There was no correlation between the levels of uric acid with the incidence of acute heart failure in patients with hypertension.Keywords: uricacid, hypertension, acute heart failureAbstrak: Hipertensi yang lama menyebabkan terjadinya pembesaran otot jantung sehingga berdampak pada terjadinya gagal jantung. Peningkatan asam urat juga menyebabkan disfungsi endotel akibat produksi reactive oxygen species (ROS) yang berlebihan, penurunan jumlah nitric oxide(NO), produksi renin meningkat, dan terjadinya reaksi inflamasi. Hal ini mempercepat perburukan otot jantung sehingga terjadi fase akut gagal jantung. Untuk mengetahui hubunganantara kadar asam urat dengan kejadian gagal jantung akut pada pasien hipertensidi instalasi rawat daruratdan poliklinik hipertensi RSUP Prof. Dr. R.D Kandou Manado. Jenis Penelitian ini adalah observasi analitik dengan menggunakan rancangan penelitian potong lintang. Dengan menggunakan metode non-probability sampling didapatkan 40 orang sebagai sampel yang telah didiagnosis menderita gagal jantung akibat hipertensi dimana 15 sampel yang mengalami episode akut dan 25 sampel yang tidak mengalami gagal jantung akut. Hasil Uji Regresi Logistik menyatakan bahwa tidak ada pengaruh yang signifikan antara kadar asam urat dengan kejadian gagal jantung akut (p=0,188), dengan nilai odds ratio sebesar 1,198. Simpulan: Tidak terdapat hubungan antara kadar asam urat dengan kejadian gagal jantung akut pada pasien hipertensi.Abstract: Long period of hypertension causes enlargement of the heart muscle, which leads to heart failure. Increased uric acid will causes endothelial dysfunction nas a result of the over production of reactive oxygen species (ROS), decrease the amount of nitric oxide (NO), increased rennin production, and the occurrence of inflammatory reactions. This speeds up the deterioration of the heart muscle, causing acute phase of heart failure. This study aimed to determine the relationship between uric acid levels and the incidence of acute heart failure in hypertensive patients in the emergency department and hypertension clinic of Prof. Dr R.D Kandou Hospital in Manado. This was an analytical observation by using the cross-sectional design. By using a non-probability sampling method we found 40 people as samples who had been diagnosed with heart failure due to hypertension. There were 15 samples that had experienced acute heart failure and 25 samples did not. Logistic Regression Test results stated that there was no significant effect of uric acid level with the incidence of acute heart failure (p = 0.188), with the value of the odds ratio of 1.198. Conclusion: There was no correlation between the levels of uric acid with the incidence of acute heart failure in patients with hypertension.Keywords: uricacid, hypertension, acute heart failureAbstrak: Hipertensi yang lama menyebabkan terjadinya pembesaran otot jantung sehingga berdampak pada terjadinya gagal jantung. Peningkatan asam urat juga menyebabkan disfungsi endotel akibat produksi reactive oxygen species (ROS) yang berlebihan, penurunan jumlah nitric oxide(NO), produksi renin meningkat, dan terjadinya reaksi inflamasi. Hal ini mempercepat perburukan otot jantung sehingga terjadi fase akut gagal jantung. Untuk mengetahui hubunganantara kadar asam urat dengan kejadian gagal jantung akut pada pasien hipertensidi instalasi rawat daruratdan poliklinik hipertensi RSUP Prof. Dr. R.D Kandou Manado. Jenis Penelitian ini adalah observasi analitik dengan menggunakan rancangan penelitian potong lintang. Dengan menggunakan metode non-probability sampling didapatkan 40 orang sebagai sampel yang telah didiagnosis menderita gagal jantung akibat hipertensi dimana 15 sampel yang mengalami episode akut dan 25 sampel yang tidak mengalami gagal jantung akut. Hasil Uji Regresi Logistik menyatakan bahwa tidak ada pengaruh yang signifikan antara kadar asam urat dengan kejadian gagal jantung akut (p=0,188), dengan nilai odds ratio sebesar 1,198. Simpulan: Tidak terdapat hubungan antara kadar asam urat dengan kejadian gagal jantung akut pada pasien hipertensi.Kata kunci: asam urat, hipertensi, gagal jantung akut: asam urat, hipertensi, gagal jantung akut

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