ライフサイエンスコーパス: oxygen glucose deprivation

1 protective in paradigms of NMDA toxicity and oxygen glucose deprivation.

2 otoxic insult (50 microM kainic acid) or 6-h oxygen glucose deprivation.

3 res, IPC and lethal ischemia were induced by oxygen-glucose deprivation.

4 t to calpain cleavage was not released after oxygen-glucose deprivation.

5 termination of SD caused by K+ perfusion and oxygen-glucose deprivation.

6 ng both middle cerebral artery occlusion and oxygen-glucose deprivation.

7 amplified by RT-PCR 24-48 hr after sublethal oxygen-glucose deprivation.

8 and maintained dendritic arborization after oxygen-glucose deprivation.

9 horylation promotes neuronal death following oxygen-glucose deprivation.

10 cal C1q(-/-) neurons exhibited resistance to oxygen-glucose deprivation.

11 protect against glutamate excitotoxicity or oxygen-glucose deprivation.

12 s monitored in hippocampal slices exposed to oxygen-glucose deprivation.

13 protein kinase C inhibition, DNA damage, or oxygen- glucose deprivation.

14 When subjected to oxygen-glucose deprivation (2 h), cortical neurons cultu

15 ntrols when exposed to a 45-55 min period of oxygen-glucose deprivation 24 hr later.

16 s in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induc

17 otypic hippocampal slice cultures exposed to oxygen glucose deprivation (a model of ischaemic stroke)

18 ated cells) in the recipient BECs exposed to oxygen-glucose deprivation, an in vitro model of cerebra

19 d in primary neurons subjected to hypoxia or oxygen-glucose deprivation, an in vitro model of ischemi

20 Following a 2-h oxygen glucose deprivation and a 1-h reoxygenation, NHE-

21 RNA interference reduced cell survival under oxygen glucose deprivation and after transplantation.

22 ates brain injury induced by excitotoxicity, oxygen glucose deprivation and middle cerebral artery (M

23 ity of cerebral endothelial cells exposed to oxygen glucose deprivation and reoxygenation (OGD + RO).

24 angiogenesis, and neutrophil migration using oxygen glucose deprivation and reoxygenation as in vitro

25 d P0-CNS optic nerves were more sensitive to oxygen-glucose deprivation and contained less adenosine

26 ed for protection of primary neurons against oxygen-glucose deprivation and excitotoxicity.

27 dium method in cultured neurons treated with oxygen-glucose deprivation and in mice treated with fore

28 release in neuronal cultures challenged with oxygen-glucose deprivation and in the rat model of trans

29 e used murine cells to demonstrate that both oxygen-glucose deprivation and pharmacologic unfolded pr

30 Here, we added diazepam early after oxygen-glucose deprivation and prevented the downregulat

31 ected primary neuronal cultures subjected to oxygen-glucose deprivation and reduced infarct size and

32 hr after termination of agonist exposure or oxygen-glucose deprivation and remained stable over the

33 In this study using an oxygen-glucose deprivation and reoxygenation (OGD/R) mod

34 ations to a combinatorial stress of neuronal oxygen-glucose deprivation and reoxygenation (OGD/R), wh

35 in vitro experiments, NSCs were subjected to oxygen-glucose deprivation and reoxygenation.

36 ions of S100B decreased neuronal death after oxygen-glucose deprivation, and this effect was abolishe

37 nificantly reduced ischemic cell death after oxygen-glucose deprivation, and this effect was abolishe

38 d(-/-) neurons were resistant to death after oxygen/glucose deprivation, and caspase 3 cleavage was s

39 Finally, using oxygen-glucose deprivation as an in vitro model for isch

40 ral vascular endothelial cell cultures after oxygen-glucose deprivation, as well as pioglitazone-medi

41 Here, we demonstrate that a primary oxygen glucose deprivation assay in primary cortical neu

42 After 2 h of oxygen/glucose deprivation, BID cleavage was detected in

43 After oxygen-glucose deprivation, brain endothelial cells rele

44 (2+) chelation could prevent SD triggered by oxygen/glucose deprivation but Zn(2+) accumulation did n

45 -methyl-4-isoxazolepropionic acid (AMPA), or oxygen-glucose deprivation, but the C3 regioisomer was m

46 However, oxygen-glucose deprivation caused a progressive downregu

47 urvival of preconditioned Sca-1+ cells under oxygen glucose deprivation compared with nonprecondition

48 ell swelling and cytotoxicity in response to oxygen-glucose deprivation, compared with slices from AQ

49 ition, Zn(2+)-mediated neuronal injury under oxygen-glucose deprivation conditions was also diminishe

50 eater neuroprotection from damage induced by oxygen glucose deprivation, consistent with the idea tha

51 obilizing ER stress (thapsigargin treatment, oxygen-glucose deprivation) critically depended upon sti

52 RNA-seq was used to compare the oxygen-glucose deprivation-damaged neurons before and af

53 Thus, after oxygen-glucose deprivation, diazepam may decrease neuron

54 ed whether glutamate receptor ligands affect oxygen-glucose deprivation-evoked L-glutamate efflux fro

55 Cultures "preconditioned" by sublethal oxygen-glucose deprivation exhibited 30-50% less neurona

56 Oxygen glucose deprivation-exposed neuronal media, or ce

57 , on primary rat cortical neurons exposed to oxygen-glucose deprivation followed by reoxygenation, an

58 death of primary cortical neurons exposed to oxygen-glucose deprivation followed by reoxygenation.

59 drug-free period, and then were subjected to oxygen-glucose deprivation for 10 min at 37 degrees C.

60 esent study of events during and after acute oxygen glucose deprivation highlights a possible importa

61 In injured (oxygen-glucose deprivation) hippocampal neuron cultures,

62 ll protect cultured hippocampal neurons from oxygen/glucose deprivation if introduced following an in

63 eptor agonist FTY720 did not protect against oxygen glucose deprivation in cultured neurons and did n

64 ce induced by transient ischemia in vivo, or oxygen-glucose deprivation in neuronal cultures.

65 hat after focal cerebral ischemia in vivo or oxygen-glucose deprivation in organotypic hippocampal sl

66 ocal ischemia in adult rats as well as after oxygen-glucose deprivation in PC12 cells.

67 middle cerebral artery occlusion in mice and oxygen-glucose deprivation in rat cortical neurons.

68 ion could be triggered in vitro by sublethal oxygen-glucose deprivation in rat hippocampal neuronal c

69 middle cerebral artery occlusion in vivo and oxygen-glucose deprivation in vitro, to delineate change

70 uroprotection against excitotoxic injury and oxygen/glucose deprivation in mouse neocortical neuron c

71 Oxygen-glucose deprivation induced an immediate rise in

72 uN2B resulted in more reduction of NMDA- and oxygen glucose deprivation-induced excitotoxicity as wel

73 urthermore PMNs exacerbated kainic acid- and oxygen glucose deprivation-induced neuron death by 20-30

74 It displayed neuroprotective effects against oxygen-glucose deprivation-induced cell injury in SH-SY5

75 by pioglitazone significantly inhibited both oxygen-glucose deprivation-induced cerebral vascular end

76 soflurane preconditioning did not change the oxygen-glucose deprivation-induced glutamate accumulatio

77 ective concentration [EC(50)] = 27 +/- 3 nM) oxygen/glucose deprivation-induced BBB breakdown, as dem

78 creased staurosporine-, excitotoxicity-, and oxygen/glucose deprivation-induced cell death in bax-def

79 Oxygen/glucose deprivation-induced injury in organotypic

80 bok-deficient neurons were more sensitive to oxygen/glucose deprivation-induced injury in vitro and s

81 ied astrocyte-secreted clusterin exacerbated oxygen/glucose-deprivation-induced necrotic death.

82 relevant, as a decrease in apoptosis, after oxygen-glucose deprivation, is observed in hippocampal n

83 hypoxia-induced oxidative stress, we used an oxygen/glucose deprivation neurodegeneration model that

84 e markedly protected from 60 min of combined oxygen-glucose deprivation neurotoxicity compared with w

85 We show in oxygen glucose deprivation of cortical neurons, an in vi

86 erability of neurons to cell death following oxygen glucose deprivation (OGD) and ischemia.

87 iability of microglia BV2 cells subjected to oxygen glucose deprivation (OGD) and re-oxygenation.

88 ischemia, hippocampal slices were exposed to oxygen glucose deprivation (OGD) conditions and we obser

89 nditioned with sublethal exposure to NMDA or oxygen glucose deprivation (OGD) exhibited enhanced Lck

90 ry cortical neurons (PCNs) were subjected to oxygen glucose deprivation (OGD) followed by various tre

91 We found that synaptic depression induced by oxygen glucose deprivation (OGD) was enhanced in EC slic

92 n and Bmal1 increase cellular survival after oxygen glucose deprivation (OGD) while the inhibition of

93 ippocampal slice cultures (OHSCs) exposed to oxygen glucose deprivation (OGD), and dissociated cultur

94 otects against the neuronal death induced by oxygen glucose deprivation (OGD), and whether the protec

95 hippocampal slices (both sexes) subjected to oxygen glucose deprivation (OGD), we found that Zn(2+) a

96 sing mouse hippocampal slices to study acute oxygen glucose deprivation (OGD)-triggered neurodegenera

97 ure to either sodium cyanide, kainic acid or oxygen glucose deprivation (OGD).

98 sulted in greater neuronal susceptibility to oxygen glucose deprivation (OGD).

99 in primary neuronal cell cultures following oxygen glucose deprivation (OGD).

100 ue to excessive glutamate (Glu) exposure and oxygen glucose deprivation (OGD).

101 tly protects mature primary OL cultures from oxygen glucose deprivation (OGD).

102 When B35 neurons were subjected to oxygen glucose deprivation (OGD)/reoxygenation or glutam

103 lls co-cultured with primary astrocytes from oxygen glucose deprivation (OGD)/reoxygenation stress an

104 ppocampal neurons were subjected to 8 min of oxygen-glucose deprivation (OGD) (an in vitro model for

105 o 2% isoflurane for 30min at 24h before a 1h oxygen-glucose deprivation (OGD) and a 24h simulated rep

106 astrocytes cultured alone or with neurons to oxygen-glucose deprivation (OGD) and monitored psi(m) us

107 ed cell death induced in cortical neurons by oxygen-glucose deprivation (OGD) and reoxygenation.

108 es, using response to two different insults: oxygen-glucose deprivation (OGD) and thrombin-mediated c

109 VPA for 24, 72, or 168 h and then exposed to oxygen-glucose deprivation (OGD) as an in vitro model of

110 For in vitro studies, we used a model of oxygen-glucose deprivation (OGD) followed by flow cytome

111 We used oxygen-glucose deprivation (OGD) in mouse cortical neuro

112 We show that oxygen-glucose deprivation (OGD) induced microglia proli

113 by PBI-05204 to rat brain slices damaged by oxygen-glucose deprivation (OGD) is mediated by BDNF.

114 In this study, we used the oxygen-glucose deprivation (OGD) model in the immortaliz

115 ncreased neuronal survival after exposure to oxygen-glucose deprivation (OGD) or glutamate toxicity.

116 he mechanism of cellular toxicity induced by oxygen-glucose deprivation (OGD) to simulate brain ische

117 Oxygen-glucose deprivation (OGD) was performed in cultur

118 Neuronal cultures subjected to oxygen-glucose deprivation (OGD), as experimental model

119 300 microM), as well as ischemia induced by oxygen-glucose deprivation (OGD), caused cellular edema

120 It has previously been shown that oxygen-glucose deprivation (OGD), reperfusion and interl

121 In addition, using an in vitro model of oxygen-glucose deprivation (OGD), we studied the role of

122 mediated ablation of miR-15a/16-1 diminished oxygen-glucose deprivation (OGD)-induced down-regulation

123 e that PPARdelta is significantly reduced in oxygen-glucose deprivation (OGD)-induced mouse CEC death

124 PC12 cells and primary rat neurons following oxygen-glucose deprivation (OGD).

125 Ischemia was simulated by oxygen-glucose deprivation (OGD).

126 m of MAP2 redistribution and breakdown after oxygen-glucose deprivation (OGD).

127 Ischemia can be modeled in vitro by oxygen-glucose deprivation (OGD).

128 nfolded protein stress, is also increased by oxygen-glucose deprivation (OGD).

129 rat hippocampal neurons from apoptosis after oxygen-glucose deprivation (OGD).

130 e potential (Psim) in mitochondria following oxygen-glucose deprivation (OGD).

131 lt rat hippocampal slice cultures by a brief oxygen-glucose deprivation (OGD).

132 dynamics in hippocampal slices subjected to oxygen-glucose deprivation (OGD).

133 We used oxygen-glucose deprivation (OGD)/reperfusion in mouse hi

134 ce and determined WM ischemic vulnerability [oxygen-glucose deprivation (OGD)] 72 h later, using acut

135 ippocampal slice model of cerebral ischemia [oxygen-glucose deprivation (OGD)] when present both duri

136 Here, we showed that oxygen-glucose deprivation (OGD, to simulate ischemia in

137 fluorescence self-quenching assay under both oxygen/glucose deprivation (OGD) and direct antibody-med

138 ng neurons to extreme metabolic stress using oxygen/glucose deprivation (OGD) increases GABAB1 but de

139 In contrast to NMDA treatment, oxygen/glucose deprivation (OGD) induced neurotoxicity i

140 Effects of oxygen/glucose deprivation (OGD) on subcellular elementa

141 opy, and subjected these slices to transient oxygen/glucose deprivation (OGD) that causes delayed exc

142 ulation of lipopolysaccharide (LPS), KCl and oxygen/glucose deprivation (OGD) that reflect inflammati

143 3-specific protease SENP3 is degraded during oxygen/glucose deprivation (OGD), an in vitro model of i

144 eurons during an in vitro model of ischemia, oxygen/glucose deprivation (OGD), leads to an enhanced p

145 riments, we tested the effects of EUK-207 on oxygen/glucose deprivation (OGD)-induced cell death in c

146 preconditioning protected against subsequent oxygen glucose deprivation or glutamate injury, whereas

147 ted in primary cortical neurons subjected to oxygen glucose deprivation or N-methyl-D-aspartate (NMDA

148 polarized 40 min earlier than soma following oxygen glucose deprivation/reoxygenation.

149 of glycolysis triggered upon excitotoxic and oxygen-glucose deprivation/reoxygenation models in mouse

150 efficacy of the stents was validated through oxygen-glucose deprivation/reoxygenation-injured neuron

151 ction of experimental acute stroke model via oxygen-glucose deprivation-reperfusion (OGD/R) injury.

152 ffect of ischemic preconditioning induced by oxygen-glucose deprivation requires K(ATP) and NO syntha

153 Exposure of cultured neurons to oxygen/glucose deprivation resulted in increased levels

154 B cells to oligodendrocyte cultures prior to oxygen glucose deprivation significantly enhanced oligod

155 n, and restore neuron function in rats under oxygen-glucose deprivation stress.

156 Ischemic stress elicited by oxygen-glucose deprivation suppressed TGF-beta1-induced

157 In the in vitro ischemic stroke model of oxygen-glucose deprivation, the sEVs-COCKTAIL exhibited

158 ceptor mutants are challenged with transient oxygen-glucose deprivation, they show a reduced function

159 cell injury in an oxidative stress model of oxygen-glucose deprivation through phosphatidylinositol-

160 IGF-1 for 30 minutes followed by 8 hours of oxygen glucose deprivation to assess the cytoprotective

161 rons, we also show that, under conditions of oxygen-glucose deprivation to mimic cerebral ischemia, G

162 used an in vitro model of cerebral ischemia (oxygen-glucose deprivation) to examine changes in [Cl-]i

163 Neurons exposed to NMDA, kainate, or oxygen-glucose deprivation underwent segmental dendritic

164 n-mediated decreases in cell death following oxygen-glucose deprivation were abolished in cortical cu

165 l brain slices exposed to ischemic injury by oxygen-glucose deprivation were treated with human amnio

166 ted pro-angiogenic proteins expression after oxygen-glucose deprivation, whereas lentiviral overexpre

167 Oxygen-glucose deprivation, which produces high endogeno