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Bupropion Showed Neuroprotective Impacts Against Cerebral Ischemia/Reperfusion Injury by Reducing Oxidative Stress and Inflammation.
Iran J Pharm Res
January 2025
Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Background: Cerebral ischemia/reperfusion (I/R) injury is the most prevalent form of brain stroke, affecting many patients worldwide. It is believed that oxidative stress and inflammation play major roles in the damage that occurs after the initiation of the disease.
Objectives: Therefore, for the first time, the current study aimed to investigate the neuroprotective effects of bupropion against cerebral I/R damage in a rat model.
cultured calculus bovis alleviates cerebral ischemia-reperfusion injury in rats through regulating microglial polarization and inhibiting NLRP3.
Zhejiang Da Xue Xue Bao Yi Xue Ban
March 2025
School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China.
Objectives: To investigate the effect of cultured calculus bovis (ICCB) on cerebral ischemia/reperfusion injury (CIRI) and its mechanism.
Methods: The CIRI animal model and cell model were induced by middle cerebral artery occlusion (MCAO) in Sprague Dawley rats and oxygen glucose deprivation/reperfusion (OGD/R) in BV2 cells, respectively. The CIRI of rat model was evaluated using modified neurological severity score (mNSS), brain water content, and cerebral infarction volume after 1.
Kisspeptin fiber and receptor distribution analysis suggests its potential role in central sensorial processing and behavioral state control.
J Neuroendocrinol
March 2025
Department of Physiology, School of Medicine, National Autonomous University of Mexico, Mexico City, Mexico.
Kisspeptin (KP) signaling in the brain is defined by the anatomical distribution of KP-producing neurons, their fibers, receptors, and connectivity. Technological advances have prompted a re-evaluation of these chemoanatomical aspects, originally studied in the early years after the discovery of KP and its receptor Kiss1r. Previously, we characterized (Hernández et al.
View Article and Find Full Text PDFMechanism of HDAC2 regulating Nrf2 acetylation level in neuronal ferroptosis of neonatal rats with hypoxic-ischemic brain injury.
Brain Inj
March 2025
Department of Neonatal, Wuhan Children's Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, China.
Objective: We investigated the mechanism of histone deacetylase 2 (HDAC2) modulating nuclear factor erythroid 2-related factor 2 (Nrf2) acetylation level in neuronal ferroptosis of hypoxic-ischemic brain injury (HIBI) neonatal rats.
Methods: The pathological damage and neuronal injury in the hippocampal CA1 region of HIBI neonatal rat models were assessed by HE and Nissl staining. Levels of neuron-specific enolase (NSE), glutathione peroxidase 4 (GPX4), HDAC2, Nrf2, glutathione (GSH), reactive oxygen species (ROS), malondialdehyde (MDA), active Fe, Nrf2 acetylation, and nuclear Nrf2 in hippocampal tissues were determined.
Epigallocatechin -3- gallate mitigates diazinon neurotoxicity via suppression of pro-inflammatory genes and upregulation of antioxidant pathways.
BMC Neurosci
March 2025
Department of Environmental & Interdisciplinary Sciences, College of Science, Engineering & Technology, Vascular Biology Unit, Center for Cardiovascular Diseases, COPHS, Texas Southern University, Houston, TX, USA.
Diazinon is a commonly used organophosphate (OP) insecticide especially in developing countries for the control of insect pests, however, exposure to its toxic impact especially in humans and other non-target species remains an important public health concern. The study aimed to investigate the effect of epigallocatechin -3- gallate (EGCG), abundant in green tea plants on neurobehavioural, biochemical, and pathological changes in the brain of male Wistar rats following exposure to diazinon toxicity. Sixty adult male Wistar rats were acclimatized for seven days and subsequently randomly assigned into six treatment groups as follows: Group I: Control group (0.
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