Current evidence for AMPK activation involvement on resveratrol-induced neuroprotection in cerebral ischemia

被引:33
作者
Pineda-Ramirez, Narayana [1 ]
Gutierrez Aguilar, German Fernando [1 ]
Espinoza-Rojo, Monica [2 ]
Aguilera, Penelope [1 ]
机构
[1] Inst Nacl Neurol & Neurocirugia Manuel Velasco Su, Lab Patol Vasc Cerebral, Av Insurgentes Sur 3877, Mexico City 14269, DF, Mexico
[2] Univ Autonoma Guerrero, Lab Biol Mol & Genom, Chilpancingo 39087, Guerrero, Mexico
关键词
Resveratrol; AMP-activated protein kinase; Cerebral ischemia; Energy metabolism; Antioxidants; PROTEIN-KINASE AMPK; ADENOSINE-MONOPHOSPHATE; OXIDATIVE STRESS; PROVIDES NEUROPROTECTION; CELL-DEATH; ISCHEMIA/REPERFUSION INJURY; METFORMIN TREATMENT; FOREBRAIN ISCHEMIA; REPERFUSION INJURY; METABOLIC-CONTROL;
D O I
10.1080/1028415X.2017.1284361
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Objectives: Cerebral ischemia is a neurological condition in which energetics and oxidative stress are dysregulated. Resveratrol is a stilbene with potent pharmacological effects associated with its antioxidant properties. In the brain, resveratrol produces protective responses against ischemia, decreases infarct volume and improves neurological function. Adenosine monophosphate-activated protein kinase (AMPK) is a cellular sensor that acts as a switch to initiate adaptive changes in response to fluctuations in energy metabolism. Results: In ischemia, AMPK is activated, nevertheless conflicting results about its contribution to protection have become apparent, and this matter continues without resolution. Interestingly, AMPK activation by resveratrol has been implicated in regulating cell survival in different experimental models. Although resveratrol's ability to regulate AMPK directly or after signaling is only beginning to be understood, targeting this enzyme by resveratrol in brain suggest that it could contribute to the amelioration of some pathologic features induced after an energetic deficit. Conclusion: The present review discusses the potential role of resveratrol in regulating AMPK activity on brain before, during, or after ischemia and offer suggestions for feasible future studies.
引用
收藏
页码:229 / 247
页数:19
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