Preconditioning with sevoflurane ameliorates spatial learning and memory deficit after focal cerebral ischemia–reperfusion in rats

2013 ◽  
Vol 31 (5) ◽  
pp. 328-333 ◽  
Author(s):  
Xianwen Hu ◽  
Ye Zhang ◽  
Weiyan Li ◽  
Jian Liu ◽  
Yun Li
2013 ◽  
Vol 41 (06) ◽  
pp. 1329-1341 ◽  
Author(s):  
Bo Yin ◽  
Hui Liang ◽  
Yigang Chen ◽  
Ketan Chu ◽  
Li Huang ◽  
...  

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.


Author(s):  
Massomeh Mohammadi ◽  
◽  
Ali Haeri-Rohani ◽  
Parichehr Yaghmaei ◽  
Hedayat Sahraei ◽  
...  

Introduction: In the present study, the effects of prenatal stress on spatial learning and memory deficit and its relationship with hippocampal insulin resistance was examined in male and female offspring. Method: Female NMRI mice were mate with males overnight and the zero day of pregnancy was detected (Gestational day zero-GD0). The pregnant mice were then randomly divided into stress and control groups. The stress group received stress from the GD0 to GD10. On post natal day 30 (PND30) the offspring were divided into for subgroups namely: male-control, female-control, male-stress, and female-stress. Barnes maze (BM) method was used for spatial learning evaluation. Plasma cortisol and insulin levels were measured at the beginning of the experiments. At the end of the experiments, the animals’ brains were removed and their hippocampus was extracted. The hippocampus was homogenized and its insulin and insulin receptor contents were evaluated. Results: The stressed animals needed more time for reaching to target hole. In addition, they spend more distance for finding the target hole, which was more pronounced in the male offspring. Both plasma and hippocampal insulin content were reduced in stressed groups. Moreover, the hippocampal insulin receptors protein was reduced in the stressed animals. There was a positive relationship between plasma and hippocampal content and memory deficit in the stressed groups. Conclusion: These results indicated that prenatal stress can induce spatial learning and memory deficit in offspring which is associated with plasma and hippocampal insulin and receptor content reduction (hippocampal insulin resistance) in these animals.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yongli Zhang ◽  
Chun-ling Dai ◽  
Yanxing Chen ◽  
Khalid Iqbal ◽  
Fei Liu ◽  
...  

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