To Use or Not to Use Metformin in Cerebral Ischemia: A Review of the Application of Metformin in Stroke Rodents

Arbeláez-Quintero, Isaac; Palacios, Mauricio

doi:10.1155/2017/9756429

Cited by 32 publications

(24 citation statements)

References 88 publications

(127 reference statements)

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“…Saeedi et al also demonstrated that metformin inhibited inflammatory cytokines, oxidative stress and necrosis by acetaminophen-induced hepatotoxicity in mice through hepatocytes protection and an antiinflammation and antioxidative mechanism (42). There is clear evidence that metformin can decrease cell death in cerebral ischemia (43). In recent studies metformin was able to conduct AMPK in the experimental cerebral ischemia, suppress inflammation pathways, protect cells through antioxidant pathways throw increased the level of catalase activities and glutathione (43).…”

Section: The Novel Beneficial Effectsmentioning

confidence: 99%

Administration of metformin in clinical medicine; an updated mini-review on current findings

Hedaiaty

2018

J Nephropharmacol

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Metformin is in the biguanide class that has been considered as the treatment for insulin resistance diabetes and polycystic ovarian disease. Many mechanisms have been suggested for it such as inhibition of the mitochondrial respiratory chain and mitochondrial glycerophosphate dehydrogenase, activation of adenosine monophosphate-activated protein kinase, inhibition of glucagon-induced elevation of cyclic adenosine monophosphate with reduced activation of protein kinase A, an effect on gut microbiota and activation of adenosine monophosphateactivated protein kinase. Metformin is a suppressor for transforming growth factor-β1 via directly binding and interact with transforming growth factor-β1 receptor. Lactic acidosis is one of the adverse and noxious effects of metformin. Nowadays, metformin has an important role in inflammation pathways and antioxidant pathways that can prevent or decrease kidney fibrosis, cardiac remodeling in hypertensive heart disease, and cell death in cerebral ischemia, kidney crystal formation, immunological diseases and cancer. Although there has been strong evidence for the potential harm caused by metformin, several studies have shown beneficial effects for it. Hence, it is necessary to revision and modification in contraindications for prescription of this drug

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Section: The Novel Beneficial Effectsmentioning

confidence: 99%

Administration of metformin in clinical medicine; an updated mini-review on current findings

Hedaiaty

2018

J Nephropharmacol

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“…To mention some, metformin has been widely studied for cerebral ischemia since it possesses pleiotropic activity and modulates AMPK activation [54]. In 2016, Zhang et al administered 7 mg/kg of metformin intraperitoneally to C57BL/6 mice for 7 days, before middle cerebral artery occlusion (MCAO).…”

Section: First Neuroprotective Pharmacological and Non-pharmacologicamentioning

confidence: 99%

Available Therapeutics after a Stroke: Current and Promising Options

Martínez¹,

Saldaña²,

Arias³

2020

New Insight Into Cerebrovascular Diseases - An Updated Comprehensive Review

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Morbidity and mortality after a cerebrovascular event have increased during the past few years, even after extensive efforts have been made concerning research in prevention, acute treatment, pharmacotherapy, revascularization, and rehabilitation. The functional deficits that arise from an ischemic event are related to the increasing chronic disability that results from lower mortality rates. More people are becoming chronically disabled; currently, as much as 90% of survivors are affected and face difficulties to continue with daily life activities. In this chapter, we briefly review the pathophysiology of ischemia and immediate clinical attention to the event. We argue about the need to seek new pharmacological and nonpharmacological alternatives and discuss the most representative in the field of neuroprotection and neurorestoration. In addition, we review the most relevant dietetic strategies and physical rehabilitation therapies, all aimed at improving the survivors' quality of life.

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“…However, it remains unclear whether AMPK activation using available approaches will translate into a viable treatment strategy for PD [158]. The two cardinal pathologies of PD are the degeneration of SNc DA neurons and the accumulation of αSyn aggregates in Lewy bodies.…”

Section: Ampk Activation As a Treatment Strategy For Pdmentioning

confidence: 99%

Targeting AMPK Signaling as a Neuroprotective Strategy in Parkinson’s Disease

Curry

Stutz

Andrews

et al. 2018

JPD

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Parkinson’s disease (PD) is the second most common neurodegenerative disorder. It is characterized by the accumulation of intracellular α-synuclein aggregates and the degeneration of nigrostriatal dopaminergic neurons. While no treatment strategy has been proven to slow or halt the progression of the disease, there is mounting evidence from preclinical PD models that activation of 5’-AMP-activated protein kinase (AMPK) may have broad neuroprotective effects. Numerous dietary supplements and pharmaceuticals (e.g. metformin) that increase AMPK activity are available for use in humans, but clinical studies of their effects in PD patients are limited. AMPK is an evolutionarily conserved serine/threonine kinase that is activated by falling energy levels and functions to restore cellular energy balance. However, in response to certain cellular stressors, AMPK activation may exacerbate neuronal atrophy and cell death. This review describes the regulation and functions of AMPK, evaluates the controversies in the field, and assesses the potential of targeting AMPK signaling as a neuroprotective treatment for PD.

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To Use or Not to Use Metformin in Cerebral Ischemia: A Review of the Application of Metformin in Stroke Rodents

Cited by 32 publications

References 88 publications

Administration of metformin in clinical medicine; an updated mini-review on current findings

Administration of metformin in clinical medicine; an updated mini-review on current findings

Available Therapeutics after a Stroke: Current and Promising Options

Targeting AMPK Signaling as a Neuroprotective Strategy in Parkinson’s Disease

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