Ischemic preconditioning-induced neuroprotection against transient cerebral ischemic damage via attenuating ubiquitin aggregation

Lee, Jae Chul; Kim, In Hye; Cho, Geum-Sil; Park, Joon Ha; Ahn, Ji Hyeon; Yan, Bing Chun; Kwon, Hyuk Min; Kim, Young‐Myeong; Cheon, Seung Hwan; Cho, Jun Hwi; Lee, Hui Young; Won, Moo‐Ho; Seo, Jeong Yeol

doi:10.1016/j.jns.2013.10.010

Cited by 25 publications

(26 citation statements)

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“…This finding has already been reported by us [23]. IPC developed by a brief time (2 min) of transient cerebral ischemia does not result in pyramidal neuronal death in the CA1 region in the gerbil, and the IPC protects CA1 pyramidal neurons from lethal transient ischemic damage following a subsequent longer duration (5 min) of transient cerebral ischemia.…”

Section: Discussionsupporting

confidence: 89%

“…IPC developed by a brief time (2 min) of transient cerebral ischemia does not result in pyramidal neuronal death in the CA1 region in the gerbil, and the IPC protects CA1 pyramidal neurons from lethal transient ischemic damage following a subsequent longer duration (5 min) of transient cerebral ischemia. It has been reported that IPC generates neuronal tolerance to a subsequent longer or lethal period of ischemia [31,32], although the time and interval of IPC has been determined by many researchers [7,23,33]. In this study, IPC induced by 2 min transient ischemia protected the CA1 pyramidal neurons from lethal transient ischemic damage induced by 5 min transient ischemia.…”

Section: Discussionmentioning

confidence: 64%

“…We carried out data analysis as follows as previously described [23]. The studied tissue sections were selected with 120 lm interval according to anatomical landmarks corresponding to anterior posterior (AP) -1.4 to -1.8 mm of the gerbil brain atlas, and cell counts were obtained by averaging the counts from 20 sections taken from each animal.…”

Section: Discussionmentioning

confidence: 99%

“…According to our previous method [23], the hippocampi were transversely cut into 400 lm thicknesses on a vibratome (Leica), and the hippocampal CA1 region was dissected with a surgical blade. The tissues were homogenized in 50 mM PBS (pH 7.4) containing 0.1 mM ethylene glycol bis (2-aminoethyl Ether)-N,N,N',N' tetraacetic acid (EGTA) (pH 8.0), 0.2 % Nonidet P-40, 10 mM ethylendiamine tetraacetic acid (EDTA) (pH 8.0), 15 mM sodium pyrophosphate, 100 mM b-glycerophosphate, 50 mM NaF, 150 mM NaCl, 2 mM sodium orthovanadate, 1 mM phenylmethylsulfonyl fluoride (PMSF) and 1 mM dithiothreitol (DTT).…”

Section: Western Blot Analysismentioning

confidence: 99%

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Neuroprotection of Ischemic Preconditioning is Mediated by Anti-inflammatory, Not Pro-inflammatory, Cytokines in the Gerbil Hippocampus Induced by a Subsequent Lethal Transient Cerebral Ischemia

et al. 2015

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Ischemic preconditioning (IPC) induced by sublethal transient cerebral ischemia could reduce neuronal damage/death following a subsequent lethal transient cerebral ischemia. We, in this study, compared expressions of interleukin (IL)-2 and tumor necrosis factor (TNF)-α as pro-inflammatory cytokines, and IL-4 and IL-13 as anti-inflammatory cytokines in the gerbil hippocampal CA1 region between animals with lethal ischemia and ones with IPC followed by lethal ischemia. In the animals with lethal ischemia, pyramidal neurons in the stratum pyramidale (SP) of the hippocampal CA1 region were dead at 5 days post-ischemia; however, IPC protected the CA1 pyramidal neurons from lethal ischemic injury. Expressions of all cytokines were significantly decreased in the SP after lethal ischemia and hardly detected in the SP at 5 days post-ischemia because the CA1 pyramidal neurons were dead. IPC increased expressions of anti-inflammatory cytokines (IL-4 and IL-13) in the stratum pyramidale of the CA1 region following no lethal ischemia (sham-operation), and the increased expressions of IL-4 and IL-13 by IPC were continuously maintained is the SP of the CA1 region after lethal ischemia. However, pro-inflammatory cytokines (IL-2 and TNF-α) in the SP of the CA1 region were similar those in the sham-operated animals with IPC, and the IL-4 and IL-13 expressions in the SP were maintained after lethal ischemia. In conclusion, this study shows that anti-inflammatory cytokines significantly increased and longer maintained by IPC and this might be closely associated with neuroprotection after lethal transient cerebral ischemia.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionmentioning

confidence: 64%

Section: Discussionmentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

See 2 more Smart Citations

Neuroprotection of Ischemic Preconditioning is Mediated by Anti-inflammatory, Not Pro-inflammatory, Cytokines in the Gerbil Hippocampus Induced by a Subsequent Lethal Transient Cerebral Ischemia

et al. 2015

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“…To investigate the delayed neuronal damage in the hippocampus after ischemia-reperfusion, F-J B histofluorescence staining was performed as previously described [19]. In brief, the sections were immersed in a 0.0004% F-J B (Histochem, Jefferson, AR, USA) staining solution.…”

Section: Fluoro-jade B (F-j B) Histofluorescencementioning

confidence: 99%

Hyperthermic preconditioning severely accelerates neuronal damage in the gerbil ischemic hippocampal dentate gyrus via decreasing SODs expressions

Kim

Cho

et al. 2015

Journal of the Neurological Sciences

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Brain ischemic preconditioning protects against moderate, not severe, transient global cerebral ischemic injury

et al. 2018

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Ischemic preconditioning (IPC) in the brain increases ischemic tolerance to subsequent ischemic insults. In this study, we examined whether IPC protects neurons and attenuates microgliosis or not in the hippocampus following severe transient global cerebral ischemia (TCI) in gerbils. Gerbils were assigned to 8 groups; 5- and 15-min sham operated groups, 5-min and 15-min TCI operated groups, IPC plus 5- and 15-min sham operated groups, and IPC plus 5- and 15-min TCI operated groups. IPC was induced by subjecting animals to 2-min transient ischemia 1 day before 5-min TCI for a typical transient ischemia and 15-min TCI for severe transient ischemia. Neuronal damage was examined by cresyl violet staining and Fluoro-Jade B histofluorescence staining. In addition, microglial activation was examined using immunohistochemistry for Iba-1 (a marker for microglia). Delayed neuronal death and microgliosis was found in the CA1 alone in the 5-min TCI operated group at 5 days post-ischemia, and, in the 15-min TCI operated group, neuronal death and microgliosis was shown in all CA areas (CA1-3) and the dentate gyrus. IPC displayed neuroprotection and attenuated microglial activation in the 5-min TCI operated group. However, in the 15-min TCI operated group, IPC did not show neuroprotection and not attenuate microglial activation. Our present findings indicate that IPC hardly protect against severe transient cerebral ischemic injury.

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Ischemic preconditioning-induced neuroprotection against transient cerebral ischemic damage via attenuating ubiquitin aggregation

Cited by 25 publications

References 50 publications

Neuroprotection of Ischemic Preconditioning is Mediated by Anti-inflammatory, Not Pro-inflammatory, Cytokines in the Gerbil Hippocampus Induced by a Subsequent Lethal Transient Cerebral Ischemia

Neuroprotection of Ischemic Preconditioning is Mediated by Anti-inflammatory, Not Pro-inflammatory, Cytokines in the Gerbil Hippocampus Induced by a Subsequent Lethal Transient Cerebral Ischemia

Hyperthermic preconditioning severely accelerates neuronal damage in the gerbil ischemic hippocampal dentate gyrus via decreasing SODs expressions

Brain ischemic preconditioning protects against moderate, not severe, transient global cerebral ischemic injury

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