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Neuroapoptosis

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https://www.readbyqxmd.com/read/28173746/neurodegenerative-changes-and-neuroapoptosis-induced-by-systemic-lipopolysaccharide-administration-are-reversed-by-dexmedetomidine-treatment-in-mice
#1
Qiaoqing Ning, Zhaoguo Liu, Xiuhua Wang, Ruyi Zhang, Jing Zhang, Meizi Yang, Hongliu Sun, Fang Han, Wenxiang Zhao, Xiuli Zhang
BACKGROUND: Sepsis-associated encephalopathy (SAE) is a frequent and nasty complication of sepsis, associated with patients increased risk of death and long-term brain dysfunctions. OBJECTIVE: This study aimed to explore the effect of dexmedetomidine (Dex), an anesthetic adjuvant, on the development of SAE. METHODS: Lipopolysaccharide (LPS, 10 mg/kg) was intraperitoneally injected to male BALB/c mice to induce sepsis. Dex (25 μg/kg) was given intraperitoneally immediately after LPS injection...
February 8, 2017: Neurological Research
https://www.readbyqxmd.com/read/28062893/prenatal-alcohol-induced-neuroapoptosis-in-rat-brain-cerebral-cortex-protective-effect-of-folic-acid-and-betaine
#2
Ibrahim Sogut, Onur Uysal, Aysegul Oglakci, Ferruh Yucel, Kazim Kartkaya, Gungor Kanbak
PURPOSE: Alcohol consumption in pregnancy may cause fetal alcohol syndrome (FAS) in the infant. This study aims to investigate prenatal alcohol exposure related neuroapoptosis on the cerebral cortex tissues of newborn rats and possible neuroprotective effects of betaine, folic acid, and combined therapy. METHODS: Pregnant rats were divided into five experimental groups: control, ethanol, ethanol + betaine, ethanol + folic acid, and ethanol + betaine + folic acid combined therapy groups...
January 6, 2017: Child's Nervous System: ChNS: Official Journal of the International Society for Pediatric Neurosurgery
https://www.readbyqxmd.com/read/28056424/neonatal-anesthetic-neurotoxicity-insight-into-the-molecular-mechanisms-of-long-term-neurocognitive-deficits
#3
REVIEW
Deshui Yu, Linji Li, Weiguo Yuan
Mounting animal studies have demonstrated that almost all the clinically used general anesthetics could induce widespread neuroapoptosis in the immature brain. Alarmingly, some published findings have reported long-term neurocognitive deficits in response to early anesthesia exposure which deeply stresses the potential seriousness of developmental anesthetic neurotoxicity. However, the connection between anesthesia induced neuroapoptosis and subsequent neurocognitive deficits remains controversial. It should be noted that developmental anesthesia related neurotoxicity is not limited to neuroapoptosis...
January 2, 2017: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
https://www.readbyqxmd.com/read/27981535/remote-ischemic-preconditioning-provides-neuroprotection-impact-on-ketamine-induced-neuroapoptosis-in-the-developing-rat-brain
#4
W Ma, Y-Y Cao, S Qu, S-S Ma, J-Z Wang, L-Q Deng, W-J Yuan, J-H Meng
OBJECTIVE: Previous studies have demonstrated that the commonly used anesthetic ketamine can acutely increase apoptosis and have long-lasting detrimental effects on cognitive function as the animal matures. Remote ischemic preconditioning (RIPC) has been confirmed to have a cerebral protective role in animal models of brain damage. The aim of this study was to investigate whether RIPC can protect the developing brain from anesthetic-induced neurotoxicity. MATERIALS AND METHODS: To investigate the protective properties of RIPC, 60 new-born Sprague-Dawley (SD) rats were randomly allocated into four groups: ketamine (20 mg/kg was diluted in saline, six times at an interval of 2 hours); RIPC (left hind row ischemia 5 min, reperfusion 5 min, a total of four cycles); ketamine + RIPC: RIPC was induced at postnatal day 5 and rats underwent the same treatment with the ketamine group after 48 hours; and saline (group vehicle)...
December 2016: European Review for Medical and Pharmacological Sciences
https://www.readbyqxmd.com/read/27959401/midazolam-anesthesia-protects-neuronal-cells-from-oxidative-stress-induced-death-via-activation-of-the-jnk-erk-pathway
#5
Jing-Yu Liu, Feng Guo, Hong-Ling Wu, Ying Wang, Jin-Shan Liu
Midazolam is an anesthetic agent commonly used during clinical and surgical procedures, which has been shown to exert ROS‑suppressing and apoptosis‑modulating pharmacological activities in various cellular systems. However, the effects of midazolam on oxidative stress in neuronal cells require elucidation. The present study investigated the effects of midazolam on buthionine sulfoximine (BSO)‑ and hydrogen peroxide (H2O2)‑induced oxidative stress in primary cortical neuronal cells. In addition, the effects of midazolam on middle cerebral artery occlusion (MCAO) in mice and on ethanol‑induced neuroapoptosis in the brains of neonatal mice were determined...
January 2017: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27924651/caffeine-combined-with-sedative-anesthetic-drugs-triggers-widespread-neuroapoptosis-in-a-mouse-model-of-prematurity
#6
Omar Hoseá Cabrera, Shawn David O'Connor, Brant Stephen Swiney, Patricia Salinas-Contreras, Francesca Maria Manzella, George Townsend Taylor, Kevin Kiyoshi Noguchi
OBJECTIVES: Caffeine (CAF) and sedative/anesthetic drugs (SADs) are often coadministered to premature infants in the neonatal intensive care unit (NICU). While SAD neurotoxicity in the developing brain is well established, it is not fully clear whether CAF interacts with SADs and whether this interaction is detrimental. Using a mouse model of prematurity, we hypothesized that CAF would increase apoptotic neurotoxicity when coadministered with SADs. METHODS: Postnatal day 3 mice were treated with vehicle or 80 mg/kg CAF prior to challenge with 6 mg/kg midazolam, 40 mg/kg ketamine, or 40 μg/kg fentanyl...
December 7, 2016: Journal of Maternal-fetal & Neonatal Medicine
https://www.readbyqxmd.com/read/27918332/isoflurane-impairs-motor-function-recovery-by-increasing-neuroapoptosis-and-degeneration-during-spinal-ischemia-reperfusion-injury-in-rats
#7
Shih-Yuan Fang, Jung-Shun Lee, Jun-Neng Roan, Yu-Chuan Tsai, Chen-Fuh Lam
BACKGROUND: Spinal cord ischemia (SCI) leads to variable degrees of neurologic deficit in patients undergoing major cardiovascular surgery. The effect of intraoperative neuroprotection against SCI and the subsequent ischemia-reperfusion injury is still limited. Because isoflurane is a commonly used anesthetic agent during major operation, and its neuroprotective and neurotoxicity effects have both been discussed, this study aimed to investigate the effect of isoflurane on the spinal cord's functional recovery in a rat model of cord ischemia...
January 2017: Anesthesia and Analgesia
https://www.readbyqxmd.com/read/27895665/sugammadex-enhanced-neuronal-apoptosis-following-neonatal-sevoflurane-exposure-in-mice
#8
Maiko Satomoto, Zhongliang Sun, Yushi U Adachi, Koshi Makita
In rodents, neonatal sevoflurane exposure induces neonatal apoptosis in the brain and results in learning deficits. Sugammadex is a new selective neuromuscular blockade (NMB) binding agent that anesthesiologists can use to achieve immediate reversal of an NMB with few side effects. Given its molecular weight of 2178, sugammadex is thought to be unable to pass through the blood brain barrier (BBB). Volatile anesthetics can influence BBB opening and integrity. Therefore, we investigated whether the intraperitoneal administration of sugammadex could exacerbate neuronal damage following neonatal 2% sevoflurane exposure via changes in BBB integrity...
2016: Anesthesiology Research and Practice
https://www.readbyqxmd.com/read/27826117/neonatal-inhibition-of-na-k-2cl-cotransporter-prevents-ketamine-induced-spatial-learning-and-memory-impairments
#9
Ryan A Stevens, Brandon D Butler, Saurabh S Kokane, Andrew W Womack, Qing Lin
Prolonged ketamine exposure in neonates at anesthetic doses is known to cause long-term impairments of learning and memory. A current theoretical mechanism explains this phenomenon as being neuro-excitotoxicity mediated by compensatory upregulation of N-methyl-d-aspartate receptors (NMDARs), which then initiates widespread neuroapoptosis. Additionally, the excitatory behavior of GABAergic synaptic transmission mediated by GABAA receptors (GABAARs), occurring during the early neuronal development period, is proposed as contributing to the susceptibility of neonatal neurons to ketamine-induced injury...
November 5, 2016: Neurotoxicology and Teratology
https://www.readbyqxmd.com/read/27820974/oroxylin-a-inhibits-h2o2-induced-oxidative-stress-in-pc12-cells
#10
Qinghe Han, Haiyu Wang, Chong Xiao, Ben-Dong Fu, Chong-Tao Du
Oroxylin A, a natural flavonoid isolated from Scutellaria baicalensis, has been reported to have anti-inflammatory and antioxidant effects. However, suppression of oxidative stress and neuroapoptosis by oroxylin A is largely uninvestigated. To investigate the protective effects of oroxylin A, PC12 cells were exposed to oroxylin A and hydrogen peroxide solutions and measured. Oroxylin A significantly reduced the levels of intracellular calcium and reactive oxygen species and increased the levels of CAT and Mn/SOD...
November 7, 2016: Natural Product Research
https://www.readbyqxmd.com/read/27682474/sevoflurane-induced-endoplasmic-reticulum-stress-contributes-to-neuroapoptosis-and-bace-1-expression-in-the-developing-brain-the-role-of-eif2%C3%AE
#11
Bin Liu, Junming Xia, Yali Chen, Jun Zhang
Neonatal exposure to volatile anesthetics causes apoptotic neurodegeneration in the developing brain, possibly leading to neurocognitive deficits in adulthood. Endoplasmic reticulum (ER) stress might be associated with sevoflurane (sevo)-induced neuroapoptosis. However, the signaling pathway regulating sevo-induced neuroapoptosis is not understood. We investigated the effects of neonatal sevo exposure on ER signaling pathway activation. Seven-day-old mouse pups were divided into control (C) and sevo (S; 3 % sevo exposure, 6 h) groups...
September 28, 2016: Neurotoxicity Research
https://www.readbyqxmd.com/read/27604310/selective-cerebral-perfusion-prevents-abnormalities-in-glutamate-cycling-and-neuronal-apoptosis-in-a-model-of-infant-deep-hypothermic-circulatory-arrest-and-reperfusion
#12
Masaki Kajimoto, Dolena R Ledee, Aaron K Olson, Nancy G Isern, Isabelle Robillard-Frayne, Christine Des Rosiers, Michael A Portman
Deep hypothermic circulatory arrest is often required for the repair of complex congenital cardiac defects in infants. However, deep hypothermic circulatory arrest induces neuroapoptosis associated with later development of neurocognitive abnormalities. Selective cerebral perfusion theoretically provides superior neural protection possibly through modifications in cerebral substrate oxidation and closely integrated glutamate cycling. We tested the hypothesis that selective cerebral perfusion modulates glucose utilization, and ameliorates abnormalities in glutamate flux, which occur in association with neuroapoptosis during deep hypothermic circulatory arrest...
November 2016: Journal of Cerebral Blood Flow and Metabolism
https://www.readbyqxmd.com/read/27588101/astragaloside-iv-protects-new-born-rats-from-anesthesia-induced-apoptosis-in-the-developing-brain
#13
Jian Sun, Xiao-Ling Chen, Jin-Yu Zheng, Jian-Wei Zhou, Zheng-Liang Ma
Exposure to general anesthesia may cause severe neurotoxicity in developing brain due to neuronal apoptosis. Astragaloside IV (AS IV) has antioxidant and antiapoptosis properties; however, its effects on anesthesia-induced neuroapoptosis have not been studied. In the present study, we determined whether AS IV pre-treatment is able to reduce isoflurane exposure-induced neuroapoptosis in rats. New born rats were pre-treated with AS IV or solvent by oral gavage for three days, then exposed to isoflurane. The results showed that pre-treatment of AS IV significantly inhibited isoflurane-induced neural apoptosis in the hippocampus of new born rats, and such protection was accompanied by reduced levels of caspase-3, nuclear factor-κB activation and phosphorylated c-Jun N-terminal kinase, extracellular signal-regulated kinase and increased levels of B-cell lymphoma-2, glycogen synthase kinase-3β, Klotho and phosphorylated protein kinase B...
September 2016: Experimental and Therapeutic Medicine
https://www.readbyqxmd.com/read/27586008/isoflurane-anesthesia-exacerbates-learning-and-memory-impairment-in-zinc-deficient-app-ps1-transgenic-mice
#14
Chunsheng Feng, Ya Liu, Ye Yuan, Weiwei Cui, Feng Zheng, Yuan Ma, Meihua Piao
Zinc (Zn) is known to play crucial roles in numerous brain functions including learning and memory. Zn deficiency is believed to be widespread throughout the world, particularly in patients with Alzheimer's disease (AD). A number of studies have shown that volatile anesthetics, such as isoflurane, might be potential risk factors for the development of AD. However, whether isoflurane exposure accelerates the process of AD and cognitive impairment in AD patients with Zn deficiency is yet to be documented. The aim of the present study was to explore the effects of 1...
December 2016: Neuropharmacology
https://www.readbyqxmd.com/read/27572468/naringenin-pre-treatment-inhibits-neuroapoptosis-and-ameliorates-cognitive-impairment-in-rats-exposed-to-isoflurane-anesthesia-by-regulating-the-pi3-akt-pten-signalling-pathway-and-suppressing-nf-%C3%AE%C2%BAb-mediated-inflammation
#15
Fu-Zhou Hua, Jun Ying, Jing Zhang, Xi-Feng Wang, Yan-Hui Hu, Ying-Ping Liang, Qin Liu, Guo-Hai Xu
The volatile anaesthetic isoflurane is one of the most frequently employed general anaesthetics in neonates, children and adults. Accumulating evidence demonstrated that exposure to anaesthetics is associated with widespread neurodegeneration and cognitive impairment. Thus, the identification and development of compounds capable of preventing or reducing these adverse effects is of great clinical importance. For this purpose, the present study aimed to assess the effects of a flavonoid, naringenin, on isoflurane-induced neuroapoptosis and cognitive impairment...
October 2016: International Journal of Molecular Medicine
https://www.readbyqxmd.com/read/27537919/from-drug-induced-developmental-neuroapoptosis-to-pediatric-anesthetic-neurotoxicity-where-are-we-now
#16
REVIEW
Catherine E Creeley
The fetal and neonatal periods are critical and sensitive periods for neurodevelopment, and involve rapid brain growth in addition to natural programmed cell death (i.e., apoptosis) and synaptic pruning. Apoptosis is an important process for neurodevelopment, preventing redundant, faulty, or unused neurons from cluttering the developing brain. However, animal studies have shown massive neuronal cell death by apoptosis can also be caused by exposure to several classes of drugs, namely gamma-aminobutyric acid (GABA) agonists and N-methyl-d-aspartate (NMDA) antagonists that are commonly used in pediatric anesthesia...
August 16, 2016: Brain Sciences
https://www.readbyqxmd.com/read/27529322/dexmedetomidine-induced-neuroapoptosis-is-dependent-on-its-cumulative-dose
#17
Jia-Ren Liu, Koichi Yuki, Chongwha Baek, Xiao-Hui Han, Sulpicio G Soriano
BACKGROUND: Dexmedetomidine (DEX) has inherent neuroprotective properties that have been attributed to the activation of prosurvival kinases. However, the impact of supraclinical doses of DEX on neuroapoptosis and neuronal viability has not been determined. METHODS: Rat pups and primary neuronal cells were treated with DEX or ketamine (KET) alone or in combination. Neuroapoptosis was measured by cleaved-caspase-3 expression and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining in brain sections...
October 2016: Anesthesia and Analgesia
https://www.readbyqxmd.com/read/27498600/neuroprotective-effects-of-caffeic-acid-phenethyl-ester-against-sevoflurane%C3%A2-induced-neuronal-degeneration-in-the-hippocampus-of-neonatal-rats-involve-mapk-and-pi3k-akt-signaling-pathways
#18
Li-Yan Wang, Zhi-Jun Tang, Yu-Zeng Han
Millions of infants and children are exposed to anesthesia every year during medical care. Sevoflurane is a volatile anesthetic that is frequently used for pediatric anesthesia. However, previous reports have suggested that the administration of sevoflurane promotes neurodegeneration, raising concerns regarding the safety of its usage. The present study aimed to investigate caffeic acid phenethyl ester (CAPE) and its protective effect against sevoflurane‑induced neurotoxicity in neonatal rats. Rat pups were administered with CAPE at 10, 20 or 40 mg/kg body weight from postnatal day 1 (P1) to P15...
October 2016: Molecular Medicine Reports
https://www.readbyqxmd.com/read/27497882/neuroprotective-effects-of-kaempferide-7-o-4%C3%A2-o-acetylrhamnosyl-3-o-rutinoside-on-cerebral-ischemia-reperfusion-injury-in-rats
#19
Shuaijun Wang, Huali Xu, Ying Xin, Maowei Li, Wenwen Fu, Yuchen Wang, Zeyuan Lu, Xiaofeng Yu, Dayun Sui
In the present study, we aim to evaluate the potential neuroprotective effect and the underlying mechanism of Kaempferide-7-O-(4″-O-acetylrhamnosyl)-3-O-rutinoside (A-F-B) against cerebral I/R injury. Adult male rats were pretreated with A-F-B by intragastric administration once a day for 3 days. One hour after the third day administration, animals were subjected to 2h of transient middle cerebral artery occlusion (MCAO) followed by 24h of reperfusion. Neurological deficit, infarct volume, histopathological changes, oxidative stress-related biochemical parameters, neuronal apoptosis, apoptosis-related proteins and the expression of pro-inflammator cytokines genes were measured...
October 5, 2016: European Journal of Pharmacology
https://www.readbyqxmd.com/read/27270941/ketamine-midazolam-anesthesia-induces-total-inhibition-of-cortical-activity-in-the-brain-of-newborn-rats
#20
Yu A Lebedeva, A V Zakharova, G F Sitdikova, A L Zefirov, R N Khazipov
The effects of general anesthetics ketamine and midazolam, the drugs that cause neuroapoptosis at the early stages of CNS development, on electrical activity of the somatosensory cortex in newborn rats were studied using extracellular recording of local field potentials and action potentials of cortical neurons. Combined administration of ketamine (40 mg/kg) and midazolam (9 mg/kg) induced surgical coma and almost completely suppressed early oscillatory patterns and neuronal firing. These effects persisted over 3 h after injection of the anesthetics...
May 2016: Bulletin of Experimental Biology and Medicine
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