scholarly journals Activation of autophagy and Akt/CREB signaling play an equivalent role in the neuroprotective effect of rapamycin in neonatal hypoxia-ischemia

Autophagy ◽  
2010 ◽  
Vol 6 (3) ◽  
pp. 366-377 ◽  
Author(s):  
Silvia Carloni ◽  
Silvia Girelli ◽  
Claudia Scopa ◽  
Giuseppe Buonocore ◽  
Mariangela Longini ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

Effect of hyperbaric oxygen on apoptosis in neonatal hypoxia-ischemia rat model

2003 ◽  
Vol 95 (5) ◽  
pp. 2072-2080 ◽  
Author(s):  
John W. Calvert ◽  
Changman Zhou ◽  
Anil Nanda ◽  
John H. Zhang
Keyword(s):  
Hyperbaric Oxygen ◽  
Caspase 3 ◽  
Apoptotic Cell ◽  
Neuroprotective Effect ◽  
Parp Cleavage ◽  
Artery Ligation ◽  
Neonatal Hypoxia ◽  
Rat Pups ◽  
Hypoxia Ischemia ◽  
Expression And Activity

We have previously demonstrated that a transient exposure to hyperbaric oxygen (HBO) attenuated the neuronal injury after neonatal hypoxia-ischemia. This study was undertaken to determine whether HBO offers this neuroprotection by reducing apoptosis in injured brain tissue. Seven-day-old rat pups were subjected to unilateral carotid artery ligation followed by 2 h of hypoxia (8% oxygen). Apoptotic cell death was examined in the injured cortex and hippocampus tissue. Caspase-3 expression and activity increased at 18 and 24 h after the hypoxia-ischemia insult. At 18-48 h, poly(ADP-ribose) polymerase (PARP) cleavage occurred, which reduced the band at 116 kDa and enhanced the band at 85 kDa. There was a time-dependent increase in the number of terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL)-positive cells. A single HBO treatment (100% oxygen, 3 ATA for 1 h) 1 h after hypoxia reduced the enhanced caspase-3 expression and activity, attenuated the PARP cleavage, and decreased the number of TUNEL-positive cells observed in the cortex and hippocampus. These results suggest that the neuroprotective effect of HBO is at least partially mediated by the reduction of apoptosis.

scholarly journals Partial Neuroprotective Effect of Pretreatment with Tanshinone IIA on Neonatal Hypoxia-Ischemia Brain Damage

2005 ◽  
Vol 58 (4) ◽  
pp. 784-790 ◽  
Author(s):  
Wen Jie Xia ◽  
Mo Yang ◽  
Tai Fai Fok ◽  
Karen Li ◽  
Wood Yee Chan ◽  
...  
Keyword(s):  
Brain Damage ◽  
Neuroprotective Effect ◽  
Tanshinone Iia ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Neuronal apoptosis can be prevented by the combined therapy with melatonin and hypothermia in a neonatal rat model of hypoxic-ischemic encephalopathy

2021 ◽  
Author(s):  
Alina Mihaela Toader ◽  
Oana Hoteiuc ◽  
Cristina Bidian ◽  
Dan-Daniel Oltean ◽  
Flaviu Tabaran ◽  
...  
Keyword(s):  
Cell Death ◽  
Neuroprotective Effect ◽  
Ischemic Injury ◽  
Brain Regions ◽  
Hypoxic Ischemic Encephalopathy ◽  
Newborn Rats ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia ◽  
The Brain ◽  
Ischemic Encephalopathy

Introduction. Birth hypoxia is a leading cause of perinatal mortality and neurological morbidity, resulting in central nervous system injury. Cerebral hypoxia and ischemia can produce a severe brain damage following a typical pattern, defined by selective vulnerability of the brain regions. The neonates are most prone to hypoxic-ischemic injuries due to the lack of efficient antioxidant defense. Neonatal hypoxia–ischemia (HI) in a 7-day-old rat HI model can produce cell death by apoptotic or necrotic mechanisms. The degree of apoptotic or necrotic mechanisms responsible for cell death in neonatal hypoxia–ischemia are not very clear as yet. The form of neuronal death may also depend on the severity of ischemic injury. Necrosis predominates in more severe cases, whereas apoptosis occurs in areas with milder ischemic injury. A human study demonstrated apoptotic and necrotic forms of cell death after hypoxic injury, whereas in some brains from stillbirths, only apoptotic figures were observed. The expression of activated caspase-3 reflects the role of apoptosis in neonatal hypoxic ischemic brain injury. Objectives. The aim of this study was to evaluate the possible neuroprotective effect of melatonin and hypothermia in hypoxic-ischemic encephalopathy in newborn rats. Local damages induced by hypoxia and ischemia were assessed by evaluating the changes in terms of histology and apoptosis. Methods. The experiment was conducted on 20 newborn Wistar rats premedicated for seven days with melatonin in a dose of 20 mg/kg/day. On the 7th postnatal day (P7), the newborn rats were exposed to ischemia (by clamping the right carotid artery) and hypobaric hypoxia (8% O2 for 90 minutes) and some groups to hypothermia. Results. In this experimental model of neonatal encephalopathy, melatonin, in a dose of 20 mg/kg/day has neuroprotective effect by reducing the number of cells expressing apoptosis in Cornu Ammonis (CA) (Ammon’s Horn) CA1, CA2, CA3 and dentate gyrus of the hippocampus when combined with hypothermia. Conclusion. The results of this study prove that melatonin is protective in ischemic-hypoxic brain injuries, but the protection is conditioned in most of the brain regions (excepting cerebral cortex) by conjugation with post-injury hypothermia treatment.  

scholarly journals The Mechanism of the Neuroprotective Effect of Kynurenic Acid in the Experimental Model of Neonatal Hypoxia–Ischemia: The Link to Oxidative Stress

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1775
Author(s):  
Ewelina Bratek-Gerej ◽  
Apolonia Ziembowicz ◽  
Jakub Godlewski ◽  
Elzbieta Salinska
Keyword(s):  
Oxidative Stress ◽  
Nmda Receptor ◽  
Experimental Model ◽  
Kynurenic Acid ◽  
Neuroprotective Effect ◽  
Neuronal Loss ◽  
Nmda Receptor Antagonist ◽  
Neonatal Hypoxia ◽  
Receptor Inhibition ◽  
Hypoxia Ischemia

The over-activation of NMDA receptors and oxidative stress are important components of neonatal hypoxia–ischemia (HI). Kynurenic acid (KYNA) acts as an NMDA receptor antagonist and is known as a reactive oxygen species (ROS) scavenger, which makes it a potential therapeutic compound. This study aimed to establish the neuroprotective and antioxidant potential of KYNA in an experimental model of HI. HI on seven-day-old rats was used as an experimental model. The animals were injected i.p. with different doses of KYNA 1 h or 6 h after HI. The neuroprotective effect of KYNA was determined by the measurement of brain damage and elements of oxidative stress (ROS and glutathione (GSH) level, SOD, GPx, and catalase activity). KYNA applied 1 h after HI significantly reduced weight loss of the ischemic hemisphere, and prevented neuronal loss in the hippocampus and cortex. KYNA significantly reduced HI-increased ROS, GSH level, and antioxidant enzyme activity. Only the highest used concentration of KYNA showed neuroprotection when applied 6 h after HI. The presented results indicate induction of neuroprotection at the ROS formation stage. However, based on the presented data, it is not possible to pinpoint whether NMDA receptor inhibition or the scavenging abilities are the dominant KYNA-mediated neuroprotective mechanisms.

scholarly journals The nonerythropoietic asialoerythropoietin protects against neonatal hypoxia-ischemia as potently as erythropoietin

2004 ◽  
Vol 91 (4) ◽  
pp. 900-910 ◽  
Author(s):  
Xiaoyang Wang ◽  
Changlian Zhu ◽  
Xinhua Wang ◽  
Jens Gammeltoft Gerwien ◽  
Andre Schrattenholz ◽  
...  
Keyword(s):  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

scholarly journals Splenic Immune Cells in Experimental Neonatal Hypoxia–Ischemia

2012 ◽  
Vol 4 (2) ◽  
pp. 208-219 ◽  
Author(s):  
Nancy Fathali ◽  
Robert P. Ostrowski ◽  
Yu Hasegawa ◽  
Tim Lekic ◽  
Jiping Tang ◽  
...  
Keyword(s):  
Immune Cells ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

Neonatal hypoxia-ischemia caused mild motor dysfunction, recovered by acrobatic training, without affecting morphological structures involved in motor control in rats

2019 ◽  
Vol 1707 ◽  
pp. 27-44 ◽  
Author(s):  
Heloísa Deola Confortim ◽  
Bruna Ferrary Deniz ◽  
Wellington de Almeida ◽  
Patrícia Maidana Miguel ◽  
Loise Bronauth ◽  
...  
Keyword(s):  
Motor Control ◽  
Motor Dysfunction ◽  
Neonatal Hypoxia ◽  
Hypoxia Ischemia

Neuroprotective Effect of Long-term MgSO4 Administration After Cerebral Hypoxia-Ischemia in Newborn Rats Is Related to the Severity of Brain Damage

2007 ◽  
Vol 14 (7) ◽  
pp. 667-677 ◽  
Author(s):  
Evangelia Spandou ◽  
Vassiliki Soubasi ◽  
Stamatia Papoutsopoulou ◽  
Persefoni Augoustides-Savvopoulou ◽  
Theodoros Loizidis ◽  
...  
Keyword(s):  
Brain Damage ◽  
Neuroprotective Effect ◽  
Cerebral Hypoxia ◽  
Newborn Rats ◽  
Hypoxia Ischemia
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