scholarly journals Bmf upregulation through the AMP-activated protein kinase pathway may protect the brain from seizure-induced cell death

2013 ◽  
Vol 4 (4) ◽  
pp. e606-e606 ◽  
Author(s):  
C Moran ◽  
A Sanz-Rodriguez ◽  
A Jimenez-Pacheco ◽  
J Martinez-Villareal ◽  
R C McKiernan ◽  
...  
Keyword(s):  
Cell Death ◽  
Protein Kinase ◽  
Amp Activated Protein Kinase ◽  
The Brain ◽  
Kinase Pathway

Abstract 337: Activation of Myocardial AMP-activated Protein Kinase by Metformin Prevents Progression of Heart Failure in Dogs; Involvement of eNOS Activation

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Hideyuki Sasaki ◽  
Hiroshi Asanuma ◽  
Masashi Fujita ◽  
Hiroyuki Takahama ◽  
Masanori Asakura ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Heart Failure ◽  
Cell Death ◽  
Protein Kinase ◽  
Left Ventricular ◽  
Vehicle Group ◽  
Mrna Levels ◽  
Compound C ◽  
Amp Activated Protein Kinase

Background; Several studies have shown that metformin activates AMP-activated protein kinase (AMPK), which mediates potent cardioprotection against ischemia-reperfusion injury. AMPK is also activated in experimental failing myocardium, suggesting that activation of AMPK is beneficial for the pathophysiology of heart failure. We investigated whether metformin prevents oxidative stress-induced cell death in rat cardiomyocytes and attenuates the progression of heart failure in dogs. Methods and Results; The treatment with metformin (10 μmol/L) protected the rat cultured cardiomyocytes against cell death due to H 2 O 2 exposure (50 μmol/L) as indicated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT), TUNEL staining, and flow cytometry. These effects were blunted by an AMPK inhibitor, compound-C (20 μmol/L), suggesting that the activation of AMPK decreased the extent of apoptosis-induced cell death due to H 2 O 2 exposure. Continuous rapid ventricular pacing (230/min for 4 weeks) in dogs caused heart failure and the treatment with metformin (100 mg/kg/day PO, n=8) decreased left ventricular (LV) end-diastolic dimension (32.8±0.4 vs. 36.5±1.0 mm, p< 0.01) and pressure (11.8±1.1 vs. 22±0.9 mmHg, p< 0.01), and increased LV fractional shortening (18.6±1.8 vs. 9.6±0.7 %, p< 0.01) along with enhanced phosphorylation of AMPK and the decreased the number of TUNEL-positive cells of the LV myocardium compared with the vehicle group (n=8). Interestingly, metformin increased the protein and mRNA levels of endothelial nitric oxide synthase of the LV myocardium and plasma nitric oxide levels. Metformin improved the plasma insulin resistance without increased myocardial GLUT-4 translocation. Furthermore, the subcutaneous administration of AICAR (50 mg/kg/every other day), another AMPK activator mediated the equivalent effects to metformin, strengthening the pivotal role of AMPK in reduction of apoptosis and prevention of heart failure. Conclusions; Activation of myocardial AMPK attenuated the oxidative stress-induced cardiomyocyte apoptosis and prevented the progression of heart failure in dogs, along with eNOS activation. Thus, metformin or AICAR may be applicable as a novel therapy for heart failure.

scholarly journals Regulation of glycogen synthesis by the laforin–malin complex is modulated by the AMP-activated protein kinase pathway

2007 ◽  
Vol 17 (5) ◽  
pp. 667-678 ◽  
Author(s):  
Maria Carmen Solaz-Fuster ◽  
José Vicente Gimeno-Alcañiz ◽  
Susana Ros ◽  
Maria Elena Fernandez-Sanchez ◽  
Belen Garcia-Fojeda ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Glycogen Synthesis ◽  
Amp Activated Protein Kinase ◽  
Kinase Pathway

Polyphenols targeting diabetes via the AMP-activated protein kinase pathway; future approach to drug discovery

2019 ◽  
Vol 56 (7) ◽  
pp. 472-492 ◽  
Author(s):  
Saeideh Momtaz ◽  
Armin Salek-Maghsoudi ◽  
Amir Hossein Abdolghaffari ◽  
Eghbal Jasemi ◽  
Shamsali Rezazadeh ◽  
...  
Keyword(s):  
Drug Discovery ◽  
Protein Kinase ◽  
Amp Activated Protein Kinase ◽  
Kinase Pathway
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