Tissue kallikrein protects rat hippocampal CA1 neurons against cerebral ischemia/reperfusion-induced injury through the B2R-Raf-MEK1/2-ERK1/2 pathway

2014 ◽  
Vol 92 (5) ◽  
pp. 651-657 ◽  
Author(s):  
Zheng Wang ◽  
Xiang Han ◽  
Mei Cui ◽  
Kun Fang ◽  
Zhengyu Lu ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Tissue Kallikrein ◽  
Ca1 Neurons ◽  
Cerebral Ischemia Reperfusion ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

EGB1212 Post-treatment Ameliorates Hippocampal CA1 Neuronal Death and Memory Impairment Induced by Transient Global Cerebral Ischemia/Reperfusion

2013 ◽  
Vol 41 (06) ◽  
pp. 1329-1341 ◽  
Author(s):  
Bo Yin ◽  
Hui Liang ◽  
Yigang Chen ◽  
Ketan Chu ◽  
Li Huang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Learning And Memory ◽  
Spatial Learning ◽  
Ischemia Reperfusion ◽  
Clinical Applications ◽  
Post Treatment ◽  
Global Cerebral Ischemia ◽  
Spatial Learning And Memory ◽  
Cerebral Ischemia Reperfusion ◽  
Hippocampal Ca1

Extracts of Ginkgo biloba have been used in traditional medicines for centuries, and have potential for clinical applications in cerebral ischemia/reperfusion injury. However, standardized extracts have proven protective only as pre-treatments, and the major mechanisms of action remain unclear. We explored the potential of the novel extract EGB1212, which meets the United States Pharmacopeia (USP) 31 standardization criteria for pharmaceutical use, as a post-treatment after global cerebral ischemia/reperfusion (GCI/R) injury in a rat model. The pre-treated group was administered EGB1212 for 7 d prior to common carotid artery occlusion (i.e., ischemia, for 20 min). Post-treated rats received the same but starting 2 h after ischemia and continuing for 7 d. Seven days after GCI/R, brains of each group were processed for H&E staining of hippocampal CA1 neurons. Remaining rats underwent the Morris water maze and Y-maze tests of spatial learning and memory, beginning eight days after reperfusion. To assess hippocampal autophagy, light chain (LC)-3-I/LC3-II and Akt/pAkt were determined via a Western blot of rat hippocampi harvested 12, 24, or 72 h after reperfusion. EGB1212 pre- and post-treatments both improved neuronal survival and spatial learning and memory functions. Pre-treatment effectively reduced LC3-II levels and post-treatment resulted in significantly elevated pAkt levels. We conclude that EGB1212 exerted significant neuroprotection in GCI/R in both preventative and post-treatment settings. This extract shows great potential for clinical applications.

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

Abstract T P84: Neuroprotective Effect of Probenecid in a Rat Model of Transient Global Cerebral Ischemia-Reperfusion

Stroke ◽  
2015 ◽  
Vol 46 (suppl_1) ◽  
Author(s):  
Rui-li Wei ◽  
Yan Xu ◽  
Jing-ye Wang ◽  
Ben-yan Luo
Keyword(s):  
Cerebral Ischemia ◽  
Protective Effect ◽  
Neuronal Death ◽  
Ischemia Reperfusion ◽  
Cerebral Injury ◽  
Therapeutic Drug ◽  
Ca1 Region ◽  
Cerebral Ischemia Reperfusion ◽  
Hippocampal Ca1

Background and Purpose: Probenecid (PROB) has been used for decades to treat gouty arthritis with few side effects and recent studies revealed that it is also a specific inhibitor of pannexin-1 channel. Panx1 channel was activated by ischemic injury and inhibition of the panx1 channel maybe efficacious in stroke treatment. However, the role of PROB in cerebral ischemia /reperfusion (I/R) injury remains unclear. The aim of this study was to investigate the role of PROB in the transient global cerebral I/R injury in rats and its protective mechanisms. Methods: Twenty minutes of transient global cerebral I/R was induced using the four-vessel occlusion (4-VO) method in rats. PROB was given in the different dose, time and administration routes to verify its neuroprotective effects. Neuronal death in the hippocampal CA1 region was observed using H & E staining 7 days after ischemia. Molecular mechanisms of activation of calpain-cathepsin pathway and inflammatory cells by I/R injury were also investigated. Results: Treatment with PROB (0.1, 1 and 10 mg/kg ) 10 min before ischemia protected against I/R-induced hippocampal CA1 neuronal death significantly, and 1 mg/kg has best protective effect. Post-insult treatment 2h after reperfusion also protected against neuronal death and prolonged use for continuous 7 days could improve its protective effects compared to the single use 6h after reperfusion.Furthermore,oral administration also had protective effect. Cathepsin B expression was inceased significantly in CA-1 region after ischemia and PROB treatment could inhibit its expression. Expression of both calpain-1 and hsp70 at 1d ,2d and 3d after reperfusion were upregulated, whereas the expression of calpain-1 was inhibited and hsp70 was strengthened by pre-treatment with PROB. Prolonged PROB treatment suppressed the activation of microglia and astrocytes, reduced the number of microglia in CA1 region. Conclusions: Our study indicates that PROB protects against transient global cerebral I/R injury administrated before ischemia and even 6h after reperfusion by reducing calpain-1 expression , inhibiting lysosomal rupture and the activation of the glia, which suggests RPOB may be a promising therapeutic drug for clinical treatment of ischemic cerebral injury.

Sesamol protects hippocampal CA1 neurons and reduces neuronal infarction in global model of cerebral ischemia in rats

2020 ◽  
Vol 14 ◽  
pp. 100217
Author(s):  
Tejas Sharma ◽  
Vishal Airao ◽  
Prakruti Buch ◽  
Devendra Vaishnav ◽  
Sachin Parmar
Keyword(s):  
Cerebral Ischemia ◽  
Global Model ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

737 FK506 protects hippocampal CA1 neurons from transient cerebral ischemia

1996 ◽  
Vol 17 (4) ◽  
pp. S183
Author(s):  
T. Hashimoto ◽  
T. Kawamata ◽  
S.-Y. Niu ◽  
M. Sasaki ◽  
T. Taniguchi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Transient Cerebral Ischemia ◽  
Ca1 Neurons ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1
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