scholarly journals Potential Role of PUMA in Delayed Death of Hippocampal CA1 Neurons After Transient Global Cerebral Ischemia

Stroke ◽  
2009 ◽  
Vol 40 (2) ◽  
pp. 618-625 ◽  
Author(s):  
Kuniyasu Niizuma ◽  
Hidenori Endo ◽  
Chikako Nito ◽  
D. Jeannie Myer ◽  
Pak H. Chan
Keyword(s):  
Cerebral Ischemia ◽  
Potential Role ◽  
Global Cerebral Ischemia ◽  
Ca1 Neurons ◽  
Transient Global Cerebral Ischemia ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Delayed Death

Sodium Hydrosulfide Post-conditioning Protects Hippocampal CA1 Neurons from Neuronal Cell Injury in the Rat Model of Transient Global Cerebral Ischemia Through Activation of Extracellular-regulated Kinases Signaling

2019 ◽  
Vol 16 (2) ◽  
pp. 156-165
Author(s):  
ChengPing Bai ◽  
ChenLiang Zhao
Keyword(s):  
Cerebral Ischemia ◽  
Rat Model ◽  
Neuronal Cell ◽  
Global Cerebral Ischemia ◽  
Sodium Hydrosulfide ◽  
Ca1 Neurons ◽  
Transient Global Cerebral Ischemia ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Pre Treatment

Introduction: The effect of hydrogen sulfide (H2S) on global cerebral ischemia remains partially understood. This study aimed to investigate the neuroprotective effect of sodium hydrosulfide (NaHS, a donor of H2S) post-conditioning and its underlying mechanism in a transient global cerebral ischemia (tGCI) model. Materials & Methods: The tGCI rat model was established by the four-vessel occlusion method. Wistar rats were randomly assigned into 6 groups: sham, tGCI, tGCI +NaHS, tGCI+vehicle, tGCI+U0126 and tGCI+U0126+NaHS groups. Neurons survival was assessed by Nissl staining and NeuN immunostaining. Levels of extracellular extracellular-regulated kinases (ERK)1/2 and p-ERK1/2 were determined by western blot and immunohistochemistry (IHC). Intraperitoneal injection of NaHS (24 μmol/kg) at 24 h post-tGCI attenuated tGCI-induced decrease of the survival and NeuN-positive neurons in the hippocampal CA1 subregion. Results: Compared to the sham group, tGCI significantly up-regulated p-ERK1/2 protein at 26 and 48 h post-tGCI. NaHS post-conditioning further enhanced the phosphorylation of ERK1/2 at 26, 48 and 168 h post-tGCI. Nevertheless, U0126 (an inhibitor of MEK1/2) pre-treatment reduced the p-ERK1/2 level in both the tGCI+ U0126 group and the tGCI+ U0126+ NaHS group. IHC staining revealed that p-ERK1/2-positive cell could be observed in several hippocampal subregions of the rats receiving NaHS post-conditioning. Immunofluorescence staining showed that some neurons were double-stained with p-ERK1/2 and NeuN. Furthermore, U0126 pre-treatment significantly attenuated the protective effect of NaHS post-conditioning on the neurons survival and NeuNpositive neurons in CA1 subregion. Conclusion: These results suggested that NaHS post-conditioning can protect hippocampal CA1 neurons from tGCI-induced injury, at least partially, through activation of ERK1/2 signaling.

Transient global cerebral ischemia induces up-regulation of MLTKα in hippocampal CA1 neurons

2011 ◽  
Vol 43 (2) ◽  
pp. 187-193 ◽  
Author(s):  
Xing Su ◽  
Chang-Lai Zhu ◽  
Wei Shi ◽  
Lan-Chun Ni ◽  
Jian-Hong Shen ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Ca1 Neurons ◽  
Transient Global Cerebral Ischemia ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1
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