dihydrodiphosphopyridine nucleotide
dihydronicotinamide-adenine dinucleotide
CAS: 58-68-4
Molecular Formula: C21H29N7O14P2
dihydrodiphosphopyridine nucleotide - Names and Identifiers
| Name | dihydronicotinamide-adenine dinucleotide |
| Synonyms | Reduced form dihydrocozymase Reduced codehydrase I dihydrodiphosphopyridine nucleotide dihydronicotinamide-adenine dinucleotide 1,4-Dihydronicotinamide adenine dinucleotide Adenosine 5'-(trihydrogen diphosphate), P'→5'-ester with 1,4-dihydro-1-β-D-ribofuranosyl-3-pyridinecarboxamide [(2R,3R,4R,5R)-5-(6-aminopurin-9-yl)-3,4-dihydroxy-oxolan-2-yl]methoxy-[[(2R,3R,4R,5R)-5-(3-carbamoyl-4H-pyridin-1-yl)-3,4-dihydroxy-oxolan-2-yl]methoxy-hydroxy-phosphoryl]oxy-phosphinic acid |
| CAS | 58-68-4 |
| EINECS | 200-393-0 |
dihydrodiphosphopyridine nucleotide - Physico-chemical Properties
| Molecular Formula | C21H29N7O14P2 |
| Molar Mass | 665.44 |
| Density | 2.18±0.1 g/cm3(Predicted) |
| Boling Point | 1081.8±75.0 °C(Predicted) |
| pKa | 1.13±0.50(Predicted) |
dihydrodiphosphopyridine nucleotide - Upstream Downstream Industry
| Downstream Products | 25 MG -NICOTINAMIDE ADENINE DINUCLEOTIDEPHOSPHATE REDUCED.NA4-SALT AN.GR. |
dihydrodiphosphopyridine nucleotide - Protective Effect of Coenzyme NADH on Myocardial Ischemia Reperfusion Injury in Rats
From VIP Journal Professional Edition
Author:
Wang Xianbao ,< a href = "https://xueshu.baidu.com/usercenter/data/author?cmd=authoruri&wd=authoruri:(134 d8772dab10fc2) author:(Wang Lin)" target = "_blank"> Wang Lin ,< a href = "https://xueshu.baidu.com/usercenter/data/author?cmd=authoruri&wd=authoruri:(3 d29b958c3c93207) author:(Zhou Haiyan)" target = "_blank">/a >,< a href = "https://xueshu.baidu.com/usercenter/data/author?cmd=authoruri&wd=authoruri:(44 e8cad7c4391dbe) author:(Zhang Peixi)" target = "_blank"> Zhang Peixi ,< a href = "https://xueshu.baidu.com/usercenter/data/author?cmd=authoruri&wd=authoruri:(3 fd7d469db390a53) author:(Sun Bo)" target = "_blank"> Sun Bo
Summary:
objective to study the protective effect of reducing coenzyme (NADH) on ischemia-reperfusion myocardium. Methods Thirty-six male Wistar rats were used to prepare myocardial ischemia-reperfusion model. They were randomly divided into myocardial ischemia-reperfusion (MIR) group, blank control group and NADH treatment group with 12 rats in each group. MIR group and NADH group were respectively taken from myocardial tissue after 30 min of ischemia (T1) and 60 min of reperfusion (T2), and total superoxide dismutase (T-SOD) and malondialdehyde (MDA) were, changes of myeloperoxidase (MPO) activity (detected after 30 min and 90 min in the control group); At T2, the ventricular wall myocardium was centrifuged immediately below the left ventricular ligation line, and the apoptosis of myocardial cells was detected by in situ notch end labeling (TUNEL) mediated by terminal deoxyribonucleic acid transferase. The ultrastructural changes of myocardium were observed under light microscope and electron microscope. Results Compared with simultaneous MIR group, MDA content and MPO activity in myocardial tissue of NADH group decreased significantly after 60 min reperfusion (P0.05). T-SOD content in myocardial tissue of NADH group increased significantly after 60 min reperfusion (P0.05). Electron microscopy showed that the mitochondrial membrane in MIR group was ruptured, the cristae were severely broken, and glycogen disappeared after 60 min reperfusion. In NADH group, the mitochondrial membrane was intact, some cristae were blurred, and glycogen decreased. The apoptosis index of myocardial cells in NADH group was 6.28±0.72 significantly lower than that in MIR group 10.91±0.92(P0.05). Conclusion NADH can significantly reduce the level of lipid peroxidation after ischemia-reperfusion, inhibit the production of hydroxyl radicals, inhibit myocardial cell apoptosis, and have protective effect on myocardial ischemia-reperfusion injury.
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keywords:
Reperfusion injury; Reduced nicotinamide adenine dinucleotide; Apoptosis; Ultrastructure
DOI:
10.3969/j.issn.1002-266X.2009.18.013
cited:
Year:
2009
Last Update：2023-08-16 22:23:51
dihydrodiphosphopyridine nucleotide - Mechanism of Coenzyme NADH on Alzheimer's Disease Cell Model
From HowNet
Author:
Summary:
among neurodegenerative diseases, Alzheimer's disease (AD) has the highest incidence and is the most common type of dementia. In 1907, German physicians AloisAlzheimer described the disease as "a degenerative brain disease characterized by progressive dementia that occurs in old age and pre-old age" and named the disease-Alzheimer's disease. In the past, it was believed that it mostly occurred before the age of 60, so it was also called Alzheimer's disease or pre-senile dementia (preseniledementia), while those who developed after the age of 60 were called senile dementia (senile dementia). The intelligence, memory, feeling, orientation, reasoning and judgment ability of AD patients have irreversible degradation, which seriously endangers human health, affects the quality of life of the elderly, and causes huge losses to society and economy. It has attracted great attention from all countries in the world. Relevant research institutes have been funded second only to AIDS. AD occurs all over the world, including almost all countries, regions and different ethnic groups. With the development of aging in various countries, the population over 60 years old increases year by year, and the incidence of AD will also increase year by year. This disease and other types of dementia rank fourth among the causes of death in the elderly. At present, among 2.5 million adults in the United States, about 1% under 65 suffer from AD, about 4-6% over 65 years old, and the prevalence rate of 85 years old and above is as high as about 25%. Our country is facing the challenge of aging population, so it is urgent to study the diagnosis and treatment of AD. The general pathological changes of AD are extensive brain atrophy, also known as diffuse brain atrophy. The cause is still unknown, and the effect of drug treatment is not obvious. The main pathological changes are senile plaques (senileplaque, SP) formation, neurofibrillary tangles (Neurofibrillary Tangles, NFT), amyloid deposition in blood vessel wall and vacuolar degeneration of hippocampal pyramidal cells. Some studies suggest that excessive apoptosis may be the cause of neurodegenerative changes in AD. A large amount of β amyloid protein (β-amyloid protein, Aβ) was found in brain SP and cerebrovascular deposits of AD patients, and Aβ plays an important role in SP formation, occurrence and development of AD. At present, due to the lack of ideal AD model, the research on pathogenesis and treatment is limited. Previous studies often used primary cultured neurons to establish models. Although it is representative and specific, its application is limited due to technical difficulties, unstable culture system and long experimental period. It has been confirmed that mouse adrenal pheochromocytoma monoclonal cell line (PC12 cell line) has the characteristics of neural crest and nerve cells, can be subcultured, and the growth condition is stable. Therefore, this study uses the active fragment of Aβ, namely Aβ25-35, to induce apoptosis of PC12 cells to establish AD cell model, which lays the foundation for further study of the pathogenesis of AD and explore new therapeutic approaches. Apoptosis is an active signal-dependent process, which can be caused by many factors, such as radiation irradiation, chemotherapy drug treatment, special toxic protein generation, hypoxia, viral infection, etc. Apoptosis is a process in which a series of morphological and physiological changes occur in cells. The gradual progress of apoptosis is accompanied by gradual changes in cell function. In the process of apoptosis, the occurrence of many important events is closely related to mitochondria, including the decrease of mitochondrial membrane potential, the change of electron transport chain, the change of intracellular redox state, the release of Caspses activator and the effect of Bcl-2 genes on apoptosis
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keywords:
PC12 cells NADH ROS apoptosis antioxidant enzymes flow cytometry NGF apoptosis rate Mortality Lipid peroxidation
Degree level:
dr.
Degree year:
2005
cited:
Last Update：2023-08-16 22:23:51
dihydrodiphosphopyridine nucleotide - Protection and repair of cell damage by coenzyme NADH
From Wanfang
Author:
Summary:
to explore the coenzyme NADH to increase the level of energy metabolism, repair cell damage, improve the ability of cell stress response and reduce the toxic damage of chemotherapy drugs and radiation to normal tissues, to explore the molecular regulation mechanism of NADH cell protection, and to provide a new prevention and treatment approach for cell protection of various clinical diseases in the future.
keywords:
coenzymes; cell protection; reduced nicotinamide adenine dinucleotide
DOI:
10.3321/j.issn:0577-7402.2002.03.001
cited:
Year:
2002
Last Update：2023-08-16 22:23:51
dihydrodiphosphopyridine nucleotide - Nature
| boiling point | 1081.8±75.0 °C(Predicted) |
| density | 2.18±0.1 g/cm3(Predicted) |
| acidity coefficient (pKa) | 1.13±0.50(Predicted) |
Last Update：2024-04-10 22:29:15
dihydrodiphosphopyridine nucleotide - Reference Information
| EPA chemical substance information | information is provided by: ofmpeb.epa.gov (external link) |
Last Update：2024-04-09 21:54:55
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