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Neuronal apoptosis

Tìm thấy 18+ kết quả cho từ khóa "Neuronal apoptosis"

Hydrogen sulfide attenuates isofluraneinduced neuroapoptosis and cognitive impairment in the developing rat brain

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H 2 S mitigates neuronal apoptosis induced by 0.75%. No signs of abdominal pain or discomfort were observed after administration of NaHS or normal saline, and none of the rats died. 1A), and compared with the CON group, neuronal apoptosis was higher (Fig. 1A: d, e, f ) in both the hippocampus and cerebral cortex.

Dexmedetomidine post-conditioning attenuates cerebral ischemia following asphyxia cardiac arrest through down-regulation of apoptosis and neuroinflammation in rats

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Dex inhibited the expression of proteins related to neuronal apoptosis following CA/CPR. According to TUNEL staining, there were few positive cells in the sham group, but their percentage increased after CA/CPR (Fig. The proportion of TUNEL-positive neurons was done by cell counting in a single field of view, which showed that the apoptosis index of CA/CPR rats was significantly increased, while Dex effectively blocked this increase (Fig.

Chapter 097. Paraneoplastic Neurologic Syndromes (Part 2)

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The target antigens are usually intracellular proteins with roles in neuronal development and function. Some of the antibodies react with epitopes located in critical protein domains, disrupting protein function and leading to neuronal apoptosis. In addition to onconeuronal antibodies, most PNDs of the CNS are associated with infiltrates of CD4+ and CD8+ T cells, microglial. Thus both humoral and cellular immune mechanisms participate in the pathogenesis of many PNDs.

Ketamine exacerbates cortical neuroapoptosis under hyperoxic conditions by upregulating expression of the Nmethyl-D-aspartate receptor subunit NR1 in the developing rat brain

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Either ketamine or hyperoxia has been reported to cause neuroapoptosis in the developing brain, and ketamine-induced neuronal apoptosis may involve a compensatory upregulation of the N-methyl-D-aspartate (NMDA) receptor NR1 subunit.. This study investigated the impact of ketamine administration under hyperoxic conditions on cortical neuroapoptosis and NR1 subunit expression in the infant rat brain..

Pretreatment with nimodipine reduces incidence of POCD by decreasing calcineurin mediated hippocampal neuroapoptosis in aged rats

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Apoptosis is a kind of active programmed cell death that occurs in the process of the development of cells in the body or under the action of some factors. Caspase-3 which is mainly involved in the process of apoptosis is the main executor of apoptosis.. Under normal circumstances, caspase-3 exists in the in- active zymogen. In the neuronal apoptosis pathway, the calcium- activated CaN activates caspase-3, which ultimately leads to neuronal apoptosis.

Neurochemical Mechanisms in Disease P32

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The cytokine-transforming growth factor-β1 (TGF-β1) may prevent neuronal apoptosis via an NF-κB-mediated mechanism, because this ability is blocked by NF- κ B decoy DNA (Zhu et al., 2004).. The roles of NF-κB in neuronal survival are complex. Mice lacking the p50 sub- unit of NF-κB exhibit increased neurotoxin-induced damage to neuronal cells as compared to wild-type mice (Yu et al., 1999), but decreased damage following a focal ischemic stroke (Nurmi et al., 2004).

Neurochemical Mechanisms in Disease P33

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Activation of NF-κB protects hip- pocampal neurons against oxidative stress-induced apoptosis (Mattson et al., 1997).. On the other hand, inhibition of NF-κB potentiates Aβ-mediated neuronal apoptosis (Kaltschmidt et al., 1999). The proapoptotic protein prostate–apoptosis response- 4 (Par-4), which is implicated in AD, kills neurons partially by inhibiting NF-κB activity (Guo et al., 1998a).

Dexmedetomidine suppresses sevoflurane anesthesia-induced neuroinflammation through activation of the PI3K/Akt/mTOR pathway

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Addition- ally, DEX has been shown to improve post-operative cognitive dysfunction in aging mice by inhibition of the hippocampal inflammatory response and reduction of neuronal apoptosis [16]. Taken together, these data sug- gest that DEX has anti-inflammatory properties in the central nervous system (CNS)..

Neurochemical Mechanisms in Disease P8

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These transgenic mice have two mutations in the human APP gene at K670N/M671L and V717I sites corresponding to β - and γ-secretase sites, respectively. in the ten-month-old APP SL /PS-1 KI mice) in the CA1 region of the hippocam- pus with an intense neuronal apoptosis (Casas et al., 2004. Page et al., 2006).

TREK-1 mediates isoflurane-induced cytotoxicity in astrocytes

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Neuron-astrocyte interactions: partnership for normal function and disease in the central nervous system. isoflurane-induced apoptosis of oligodendrocytes in the neonatal primate brain. Abuse liability of the anesthetic propofol:. Deletion of the background potassium channel TREK-1 results in a depression-resistant phenotype. Inhibition of p75 neurotrophin receptor attenuates isoflurane-mediated neuronal apoptosis in the neonatal central nervous system

The influences of morphine or ketamine pre-treatment on hemodynamic, acid-base status, biochemical markers of brain damage and early survival in rats after asphyxial cardiac arrest

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Caspase-3 is an essential protease, which is involved in the early stage of apoptosis and it is generally accepted as a hallmark of irreversible cell death [10]. Other experimental studies have shown that inhibition of the NMDA receptor by Ketamine may reduce neuronal apoptosis and attenuate the systemic inflammatory response to tissue injury [25–27].

Right stellate ganglion block improves learning and memory dysfunction and hippocampal injury in rats with sleep deprivation

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In addition, neurodegeneration, microglia activation, and neuronal apoptosis will occur in the hippocampus of mice after sleep deprivation [19]. It has been confirmed in clinical and animal experiments that sleep deprivation leads to increased white blood cell counts and elevated levels of inflammatory factors such as C-reactive protein (CRP), IL1, IL6, and TNF [20]..

Anxiolytic, antioxidant, and neuroprotective effects of goji berry polysaccharides in ovariectomized rats: experimental evidence from behavioral, biochemical, and immunohistochemical analyses

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However, the effects of different dosages of such polysaccharides on ovariectomized rats and their underlying mechanisms in the brain have not been evaluated in the literature. thus, LBP may have applications in the treatment of neuronal apoptosis induced neurodegenerative diseases (Teng et al., 2013).. Brinton et al., 2015).

Cerebral Edema Phu Nao

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Late complications include neuronal apoptosis, atrophy, and gliosis.Có sự hạn chế khuếch tán toàn bộ của các phân tử nước qua màng tế bào và bên trong nguyênsinh chất chất dẫn đến vùng tăng tín hiệu trên DWI và giảm tín hiệu trên ADC. Ban đầu, hàngrào máu - não vẫn còn nguyên vẹn và nước ngoài tế bào không tăng, mang lại sự bình thườngtrên bản đồ DTI và phân số bất đẳng hướng.

The interplay of BDNF-TrkB with NMDA receptor in propofol-induced cognition dysfunction

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However, a large number of cell experi- ments and animal studies have found that propofol can lead to cerebral neuronal apoptosis during development, and cause developmental abnormalities such as long-term learning and memory [6–8]. Learning and memory is a very com- plex process, and the molecular and cellular mechanisms are still unclear. It has been known that learning and.

High-fat diet aggravates postoperative cognitive dysfunction in aged mice

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Moraes [16] found that a HFD can induce neuronal apoptosis and promote the expression of the apoptosis markers Bax, caspase-3, caspase-6 and caspase-8 in the hypothalamus. In con- trast, in the same model, the levels of the antiapoptotic Bcl family proteins were inhibited. In our study, the hippocampal levels of the pro-apoptosis factors Bax and caspase-3 cleaved were higher in the HFC group and HFS groups compared with the ALC and ALS groups,.

Effects of resveratrol pretreatment on endoplasmic reticulum stress and cognitive function after surgery in aged mice

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Reduced AKT phosphorylation contributes to endoplasmic reticulum stress-mediated hippocampal neuronal apoptosis in rat recurrent febrile seizure. Endoplasmic reticulum stress is involved in restraint stress-induced hippocampal apoptosis and cognitive impairments in rats. The role of endoplasmic reticulum stress in neurodegenerative disease. Endoplasmic reticulum stress pathway mediates isoflurane-induced neuroapoptosis and cognitive impairments in aged rats.

Identification of differentially expressed microRNAs in primary esophageal achalasia by next-generation sequencing

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The histopathology analysis of the esophageal tissues, indicated lymphocytic infiltration, myenteric inflammation, and aganglionosis during the achalasia (Sodikoff et al., 2016). 0.840) in the esophageal tissues of the patients with achalasia compared to the controls by the quantitative reverse transcription polymerase chain reaction (qRT-PCR) validation. neuronal apoptosis in the achalasia tissues (Kahrilas and Boeckxstaens, 2013). has been reported downregulated in several cancers such as gastric

Mesenchymal stromal cells attenuate sevoflurane-induced apoptosis in human neuroglioma H4 cells

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Conclusions: Our study indicated that soluble factors secreted by MSCs attenuated the sevoflurane-induced oxidative stress and apoptosis of neuronal cells by preserving their mitochondrial function.. sevoflurane-induced oxidative stress and neuronal apop- tosis by preserving the mitochondrial function.. Hu- man neuroglioma H4 cells (H4 cells) share some similar- ities with glial cells in vitro and have been widely used for studies of neuronal impairment and apoptosis [26–28]..

Effects and mechanism of dexmedetomidine on neuronal cell injury induced by hypoxia-ischemia

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dexmedetomidine on neuronal cell injury induced by hypoxia-ischemia. Background: The present study aims to investigate the protective effects of dexmedetomidine (DMED) on hypoxia ischemia injury induced by oxygen and glucose deprivation (OGD) in PC12 and primary neuronal cells.. Methods: PC12 cells exposed to OGD was used to establish ischemia model. The OGD-induced cell injury was evaluated by alterations of cell viability, apoptosis and expressions of apoptosis-associated proteins.