Targeting Adenosine Monophosphate-Activated Protein Kinase by Metformin Adjusts Post-Ischemic Hyperemia and Extracellular Neuronal Discharge in Transient Global Cerebral Ischemia

(2015) Targeting Adenosine Monophosphate-Activated Protein Kinase by Metformin Adjusts Post-Ischemic Hyperemia and Extracellular Neuronal Discharge in Transient Global Cerebral Ischemia. Microcirculation.

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Abstract

Objective: I/R and its subsequent reactive hyperemia results in different adverse effects such as brain edema and BBB disruption. AMPK activation has been perceived as one of the target factors for I/R treatment. We investigated the effect of Met (an AMPK activator) on some physiological parameters including vascular responses, hyperemia, BBB disruption, and electrophysiological activity following tGCI. Methods: Rats were pretreated with Met for two weeks and CC was administered half an hour before tGCI. Brain vascular responses, hyperemia, BBB disruption, and electrophysiological activity were evaluated following the ischemia. Results: Met attenuated BBB disruption and reactive hyperemia in tGCI rats compared with the untreated I/R rats (p < 0.001). Met administration along with CC in the ischemic rats reversed the beneficial effects of Met on BBB disruption and reactive hyperemia (p < 0.001). Electrophysiological records indicated that Met increased spike rates in the ischemic rats comparing with I/R rats (p < 0.001), whereas, CC administration blocked the beneficial effects of Met on the neuronal discharges (p < 0.05). Conclusion: We established a regulatory role for AMPK in vascular and electrophysiological responses to tGCI. Studies are ongoing to determine if activation of AMPK in the reperfusion period would offer similar protection. © 2015 John Wiley & Sons Ltd.

Item Type: Article
Additional Information: cited By
Keywords: hydroxymethylglutaryl coenzyme A reductase kinase; metformin; hydroxymethylglutaryl coenzyme A reductase kinase; metformin, adult; animal experiment; animal model; animal tissue; Article; blood brain barrier; brain blood flow; controlled study; drug mechanism; drug targeting; enzyme activation; enzyme activity; firing rate; hyperemia; male; membrane damage; nerve cell lesion; nonhuman; priority journal; rat; transient ischemic attack; animal; blood brain barrier; brain ischemia; enzymology; metabolism; pathophysiology; Wistar rat, AMP-Activated Protein Kinases; Animals; Blood-Brain Barrier; Brain Ischemia; Hyperemia; Male; Metformin; Rats; Rats, Wistar
Subjects: biochemistry
pharmacology
Divisions: Education Vice-Chancellor Department > Faculty of Medicine > Department of Basic Science > Department of Physiology Pharmacology Medical
Depositing User: دکتر مهری غلامی
URI: http://eprints.abzums.ac.ir/id/eprint/728

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