Effects of Hypothermia on Hypoxia-Induced Apoptosis in Cultured Neurons from Developing Rat Forebrain: Comparison with Preconditioning
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Neonatal hypoxic-ischaemic encephalopathy (HIE) is major cause of neonatal mortality and morbidity. Therapeutic hypothermia is standard clinical care for moderate hypoxic-ischaemic (HI) brain injury, however it reduces the risk of death and disability only by 11% and 40% of the treated infants still develop disabilities. Thus it is necessary to develop supplementary therapies to complement therapeutic hypothermia in the treatment of neonatal HIE. The modified Rice-Vannucci model of HI in the neonatal mouse is well developed and widely applied with different periods of hypothermia used as neuroprotective strategy in combination with other agents. However, different studies use different periods, time of initiation and duration of hypothermia following HI, with subsequent varying degrees of neuroprotection. So far most rodent data is obtained using exposure to 5-6h of therapeutic hypothermia. Our aim was to compare the effect of exposure to three different short periods of hypothermia (1h, 1.5h and 2h) following HI insult in the postnatal day 7 C57/Bl6 mouse, and to determine the shortest period providing neuroprotection. Our data suggests that 1h and 1.5h of hypothermia delayed by 20min following a 60min exposure to 8%O2 do not prove neuroprotective. However, 2h of hypothermia significantly reduced tissue loss, TUNEL+ cell death and microglia and astroglia activation. We also observed improved functional outcome 7 days after HI. We suggest that the minimal period of cooling necessary to provide moderate short term neuroprotection and appropriate for the development and testing of combined treatment is 2h.
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Hypothermia therapy is an old and important method of neuroprotection. Until now, many neurological diseases such as stroke, traumatic brain injury, intracranial pressure elevation, subarachnoid hemorrhage, spinal cord injury, hepatic encephalopathy, and neonatal peripartum encephalopathy have proven to be suppressed by therapeutic hypothermia. Beneficial effects of therapeutic hypothermia have also been discovered, and progress has been made towards improving the benefits of therapeutic hypothermia further through combinations with other neuroprotective treatments and by probing the mechanism of hypothermia neuroprotection. In this review, we compare different hypothermia induction methods and provide a summarized account of the synergistic effect of hypothermia therapy with other neuroprotective treatments along with an overview of hypothermia neuroprotection mechanisms and cold/hypothermia-induced proteins.
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AIM: To compare hypoxia and hypoxia reoxygenation induced apoptosis of cardiomyocytes and to investigate the role of apoptosis in cardiomyocytes injury caused by hypoxia/reoxygenation. METHODS: Cultured neonatal rat cardiomyocytes were divided into two groups.Both groups were cultured in an incubator of 950 ml/L N 2 and 50 ml/L CO 2 for 16, 32 and 48 h. Cells of one group were put into normal incubation for 6 h after hypoxia to form the cell models of hypoxia reoxygenation injury. Morphological changes in apoptotic cardiomyocytes were measured by TUNEL staining. Apoptosis rates were measured by flow cytometer. RESULTS: Positive cells were detected by TUNEL staining. Apoptotis rates of cardiomyocytes measured by flow cytometer after hypoxia for 16,32 and 48 h were (2.9±0.5)%,(6.2±0.8)% and (26.6±3 0)% respectively.The apoptosis rates of cells undergoing hypoxia for 16,32 and 48 h followed by reoxygenation for 6 h were (5.5±0.7)%,(11.0±1.1)% and (14.2±1.6)% respectively. CONCLUSION: The apoptosis rates of cardiomyocytes increased with time of hypoxia.Reoxygenation could worsen cardiomyocytes injury,as compared with hypoxia.
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Neuronal cells are extremely vulnerable and have a limited capacity for self-repair in response to injury. For those reasons, there is obvious interest in limiting neuronal damage. Mechanisms and strategies used in order to protect against neuronal injury, apoptosis, dysfunction, and degeneration in the central nervous system are recognized as neuroprotection. Neuroprotection could be achieved through several classes of natural and synthetic neuroprotective agents. However, considering the side effects of synthetic neuroprotective agents, the search for natural neuroprotective agents has received great attention. Recently, an increasing number of studies have identified neuroprotective properties of chitosan and its derivatives; however, there are some significant challenges that must be overcome for the success of this approach. Hence, the objective of this review is to discuss neuroprotective properties of chitosan and its derivatives.
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Herbal bioactive compounds have been investigated to possess neuroprotective properties. They are involved in the modulation of different signaling pathways that may facilitate neuroprotection. In this brief review, some of the promising compounds and their potential neuroprotective effects have been reported. They can be potential sources of therapeutics for neurodegenerative disorders.
KEYWORDS: neuroprotective, herbal, bioactive compounds, neurodegenerative diseases
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Aim To study the role of hypoxiainduced apoptosis in neonatal rat cardiomyocyte and the protection effect of nitric oxide(NO). Methods Neonatal rat cardiomyocytes were cultured in an incubator of 950 mL/L N 2 and 50 mL/L CO 2 for 16, 32 and 48 h to create cell models of hypoxia injury and detect apoptosis. And NO donor SNAP at 100 μ mol/L was added to the models. Apoptosis was detected in the hypoxia cells without or with No treatment. Results After hypoxia of 16, 32 and 48 h,the apoptosis rates of cardiomyocytes were 29% ± 05% , 62% ± 08% and 266% ± 30% , respectively. Whereas the apoptosis rates of cells treated with SNAP were 02% ± 03% , 34% ± 04% and 118% ± 12% , respectively. Conclusion Apoptosis is the main form of hypoxia injury in cardiomyocytes; NO protect cardiomyocytes from apoptosis induced by hypoxia.
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