Acute administration of metformin prior to cardiac ischemia/reperfusion injury protects brain injury

Leech, Tom; Apaijai, Nattayaporn; Palee, Siripong; Higgins, Louis; Maneechote, Chayodom; Chattipakorn, Nipon

doi:10.1016/j.ejphar.2020.173418

Cited by 15 publications

(15 citation statements)

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“…1.3.3 | Alterations in Alzheimer's related proteins and synaptic protein expression Upregulation of Alzheimer's disease related proteins were associated with cognitive impairment. The evidence of BBB breakdown after cardiac ischemia are reported, 21,62 the circulating oxidative stress and inflammatory cytokines are facilitated to the brain and disrupt the cleavage of amyloid precursor protein. 15 The activity of beta secretase-1 was increased during the exposure of oxidative stress and inflammation; thus, the beta cleavage of APP was increased, together with lower amyloid beta clearance capacity in the brain, resulting in amyloid beta deposition, which is a hallmark of the AD pathogenesis.…”

Section: Inflammationmentioning

confidence: 99%

“…Several previous studies have been reported that cardiac reperfusion caused cognitive impairment as indicated by dendritic spine loss after acute 2 hours of reperfusion. 21,62,91 There is only one study reported cell death related cognitive impairment after 16 weeks of reperfusion. 38 Nevertheless, other molecular mechanism is needed for a future investigation.…”

Section: Impairment (Mci)mentioning

confidence: 99%

“…Brain mitochondrial dysfunction was observed in animal models of cardiac I/R injury, prediabetes, and Alzheimer's disease. 21,62,94,95 Despite intensive studies in both clinical and animal models have been reported the alteration of brain mitochondria in HF models. [96][97][98] However, the potential role of brain mitochondrial function in HF is rather limited.…”

Section: Future Investigationmentioning

confidence: 99%

“…20 Reduced dendritic density was reported following cardiac ischemia-reperfusion (I/R) and MI. 14,21,22 This review aims to summarize and discuss the mechanisms underlying cognitive impairment following chronic HF. Additionally, clinical reports regarding the link between cardiac function and cognitive impairment in patients with HF will be discussed.…”

Section: Introductionmentioning

confidence: 99%

“…Dendritic spines are vital elements of synaptic function and plasticity which influence the ability of learning and memory 20 . Reduced dendritic density was reported following cardiac ischemia‐reperfusion (I/R) and MI 14,21,22 . This review aims to summarize and discuss the mechanisms underlying cognitive impairment following chronic HF.…”

Section: Introductionmentioning

confidence: 99%

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Cognitive impairment in myocardial infarction and heart failure

2021

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Myocardial infarction (MI) occurs when coronary blood flow is decreased due to an obstruction/occlusion of the vessels, leading to myocardial death and progression to heart failure (HF). Cognitive impairment, anxiety, depression and memory loss are the most frequent mental health problems among patients with HF. The most common cause of cognitive decline is cardiac systolic dysfunction, which leads to reduced cerebral perfusion. Several in vivo and clinical studies provide information regarding the underlying mechanisms of HF in brain pathology. Neurohormonal activation, oxidative stress, inflammation, glial activation, dendritic spine loss and brain programmed cell death are all proposed as contributors of cognitive impairment in HF. Furthermore, several investigations into the effects of various medications on brain pathology utilizing MI models have been reported. In this review, potential mechanisms involving HF-associated cognitive impairment, as well as neuroprotective interventions in HF models, are discussed and summarized. In addition, gaps in the surrounding knowledge, including the types of brain cell death and the effects of cell death inhibitors in HF, are presented and discussed. This review provides valuable information that will suggest the potential therapeutic strategies for cognitive impairment in patients with HF.

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Section: Inflammationmentioning

confidence: 99%

Section: Impairment (Mci)mentioning

confidence: 99%

Section: Future Investigationmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Cognitive impairment in myocardial infarction and heart failure

2021

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The role of AMPK-dependent pathways in cellular and molecular mechanisms of metformin: a new perspective for treatment and prevention of diseases

Hasanvand

2022

Inflammopharmacol

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Metformin can suppress gluconeogenesis and reduce blood sugar by activating adenosine monophosphate-activated protein kinase (AMPK) and inducing small heterodimer partner (SHP) expression in the liver cells. The main mechanism of metformin’s action is related to its activation of the AMPK enzyme and regulation of the energy balance. AMPK is a heterothermic serine/threonine kinase made of a catalytic alpha subunit and two subunits of beta and a gamma regulator. This enzyme can measure the intracellular ratio of AMP/ATP. If this ratio is high, the amino acid threonine 172 available in its alpha chain would be activated by the phosphorylated liver kinase B1 (LKB1), leading to AMPK activation. Several studies have indicated that apart from its significant role in the reduction of blood glucose level, metformin activates the AMPK enzyme that in turn has various efficient impacts on the regulation of various processes, including controlling inflammatory conditions, altering the differentiation pathway of immune and non-immune cell pathways, and the amelioration of various cancers, liver diseases, inflammatory bowel disease (IBD), kidney diseases, neurological disorders, etc. Metformin’s activation of AMPK enables it to control inflammatory conditions, improve oxidative status, regulate the differentiation pathways of various cells, change the pathological process in various diseases, and finally have positive therapeutic effects on them. Due to the activation of AMPK and its role in regulating several subcellular signalling pathways, metformin can be effective in altering the cells’ proliferation and differentiation pathways and eventually in the prevention and treatment of certain diseases. Graphical abstract

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