Mechanisms of ammonia-induced cell death in rat cortical neurons: Roles of NMDA receptors and glutathione

Klejman, Agata; Węgrzynowicz, Michał; Szatmári, E; Mioduszewska, Barbara; Hetman, Michał; Albrecht, Jan

doi:10.1016/j.neuint.2005.04.006

Cited by 60 publications

(48 citation statements)

References 48 publications

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“…The symptoms of VD may correlate with the injury of cerebral cortex and hippocampus induced by the increase of free radicals. 24,32,33) Oxidative stress caused by the increase of intracellular reactive oxygen species (ROS) has been proven in relation to degenerative disorders, including premature aging, Alzheimer's disease, vascular dementia. 34,35) When cerebral neurons were attacked by excessive free radicals, the content of MDA and the activity of SOD can be increased and decreased, respectively.…”

Section: Discussionmentioning

confidence: 99%

“…As we known, oxidative stress easily produces lipid peroxidation resulting in the increase of cell death. 21,32) H 2 O 2 , one of the major component of ROS, can directly stimulate endonuclease activity in cells, leading to DNA fragmentation and cell death. 20,46) In MTT test, breviscapine relieved the cell toxicity induced by H 2 O 2 in a dosedependant manner.…”

Section: Discussionmentioning

confidence: 99%

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Protective Effects of Breviscapine on Ischemic Vascular Dementia in Rats

Xiong

Liu

Wang

et al. 2006

Biological & Pharmaceutical Bulletin

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With an increase of elderly population, aging-related diseases such as hypertension, arteriosclerosis and different forms of dementia are also increased. 1) One of these diseases is vascular dementia (VD). VD is a step-wise deterioration in intellectual powers that appear as different areas of the brain are damaged by loss of blood supply.2,3) The conventional concept of VD is that of multi-infarct dementia, 3,4) arising from chronic cerebral ischemia and various vascular changes in the brain.5) It is reported that the reduction in cerebral blood flow and abnormal energy metabolism occurred in chronic cerebral ischemia can induce the accumulation of NO and ROS which lead to neurons injury in selective, vulnerable regions of the brain, especially the hippocampus and cerebral cortex, accompanied by cognitive decline and some motor disorders. [6][7][8] In oriental medicine, many traditional Chinese drugs have been used clinically for treatment of ischemic cerebrovascular disease. 9) Breviscapine is extracted from the traditional Chinese drug Erigeron Breviscapus (vant.) Hand.-Mazz and mainly composed of Scutellarein, Plantaginin and Pyromeconic acid. 10,11) The injection preparation of breviscapine has been used in clinic to treat cardiovascular diseases, cerebral infarction and stroke in China. 3,10,11) The clinical reports suggested that the injection of breviscapine (0.5 mg/kg, i.v. gtt, qd, 15 d) possess neuroprotective action and improves learning and memory in cerebrovascular diseases.12,13) Although the curative effect of breviscapine in cerebral infarction and cerebral ischemia is obvious, there is no data available for this drug in treatment of VD. In this study, the effects of chronic treatment with breviscapine on the learning deficits, neuronal injury and antioxidative properties in VD rats were investigated. MATERIALS AND METHODS Animal Models and Drug AdministrationThe vascular dementia models were made from the male Wistar rats (6 weeks, 230Ϯ10 g), which were obtained from the Experimental Animals Center of Tongji Medical College, Huazhong University of Science and Technology. Wistar rats were subjected to permanent occlusion of bilateral common carotid arteries to induce chronic cerebral ischemia and mimic the VD models.14) The experimental protocols were approved by the Committee of Animal Care of Huazhong University of Science and Technology.The injection of breviscapine (Bre, Bath No. z5302066, China) was purchased from Kunming Long-Jin Pharmaceutical Co., Ltd. Tacrine (9-amino-1,2,3,4-tetrahydroacridine HCl), a reference drug for behavioral test, was purchased from Sigma (St. Louis, MO, U.S.A.) and dissolved in physiological saline. Fifteen days after surgery, the male Wistar rats were randomly divided into three groups, e.g., sham-operated group, model group, Bre-treated group and tacrine-treated group. The Bre-treated group was administered with breviscapine (2 mg/kg, i.p., equal 0.33 mg/kg adult dose, once a day). Tacrine was administered intraperitoneally at a dosage of 3 mg/kg. The sham-ope...

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Protective Effects of Breviscapine on Ischemic Vascular Dementia in Rats

Xiong

Liu

Wang

et al. 2006

Biological & Pharmaceutical Bulletin

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“…NR2B causes c-Jun N-terminal kinase activation in rat neurons [Guo et al, 2009], which in turn induces cell cycle arrest, resulting in an increase in the percentage of cells in the G 1 phase and a decrease in the percentage of cells in the S phase [Tao and Segil, 2015]. Furthermore, NR2B blockage by ifenprodil reduced calcium influx, which attenuates the blockade of DNA replication by calcium and maintains normal cell proliferation [Klejman et al, 2005].…”

Section: Id1/nr2b Receptor Pathway Is Involved In Oc1 Cell Radiation-mentioning

confidence: 99%

Id1/NR2B Receptor Pathway Regulates Rat Cochlear Sensory Epithelial Cell Survival after Radiation

Chen¹,

Zhou²,

Zou³

et al. 2018

Audiol Neurotol

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Survival of cochlear sensory epithelial cells may be regulated by inhibitor of differentiation-1 (Id1) and the N-methyl-D-aspartic acid (NMDA) receptor. However, it is unclear whether Id1 and the NMDA receptor are involved in the radiation-mediated survival of rat cochlear sensory epithelial cells. Here, we show that the percentage of apoptotic cells increased, the percentage of cells in the S phase decreased, Id1 mRNA and protein expression decreased and the NMDA receptor subtype 2B (NR2B) mRNA and protein level increased in OC1 cells after radiation. Cells infected with the Id1 gene exhibited higher Id1 mRNA and protein levels and lower NR2B mRNA and protein levels than the control cells. In contrast, after transfection of the Id1 siRNA into OC1 cells, Id1 mRNA and protein expression decreased and NR2B mRNA and protein expression increased relative to that of the control group. Additionally, treatment with ifenprodil for 24 h before radiation reduced apoptosis and increased the percentage of cells in the S phase. Our results suggest that Id1 and NR2B might regulate the survival of OC1 cells following radiation.

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“…Effects of ammonia were observed not only in plant-fungal interactions: Coccidioides immitis, a fungal pathogen of humans that causes respiratory disease, is known to alkalinize its environment with ammonia (36, 73, 97); mutants with compromised ammonia secretion were less pathogenic (98), and ammonia was shown to compromise the rat-host immune response and cause inflammation (67). Further, in rat astrocytes and brain edema ammonia was shown to activate NADPH oxidase, which was followed by autophagy (17, 31, 68,71,74,75,105,125,133), which suggests that ammonia possesses a global role of action on NADPH oxidase and cell death.…”

Section: Host Response To Ammoniamentioning

confidence: 99%

Virulence Regulation of Phytopathogenic Fungi by pH

Alkan

Espeso

Prusky³

2013

Antioxidants & Redox Signaling

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Significance: Postharvest pathogens can start its attack process immediately after spores land on wounded tissue, whereas other pathogens can forcibly breach the unripe fruit cuticle and then remain quiescent for months until fruit ripens and then cause major losses. Recent Advances: Postharvest fungal pathogens activate their development by secreting organic acids or ammonia that acidify or alkalinize the host ambient surroundings. Critical Issues: These fungal pH modulations of host environment regulate an arsenal of enzymes to increase fungal pathogenicity. This arsenal includes genes and processes that compromise host defenses, contribute to intracellular signaling, produce cell wall-degrading enzymes, regulate specific transporters, induce redox protectant systems, and generate factors needed by the pathogen to effectively cope with the hostile environment found within the host. Further, evidence is accumulating that the secreted molecules (organic acids and ammonia) are multifunctional and together with effect of the ambient pH, they activate virulence factors and simultaneously hijack the plant defense response and induce program cell death to further enhance their necrotrophic attack. Future Directions: Global studies of the effect of secreted molecules on fruit pathogen interaction, will determine the importance of these molecules on quiescence release and the initiation of fungal colonization leading to fruit and vegetable losses.

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Mechanisms of ammonia-induced cell death in rat cortical neurons: Roles of NMDA receptors and glutathione

Cited by 60 publications

References 48 publications

Protective Effects of Breviscapine on Ischemic Vascular Dementia in Rats

Protective Effects of Breviscapine on Ischemic Vascular Dementia in Rats

Id1/NR2B Receptor Pathway Regulates Rat Cochlear Sensory Epithelial Cell Survival after Radiation

Virulence Regulation of Phytopathogenic Fungi by pH

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