Propranolol and low-dose isoproterenol ameliorate insulin resistance, enhance β-arrestin2 signaling, and reduce cardiac remodeling in high-fructose, high-fat diet-fed mice: Comparative study with metformin

Ibrahim, Wael; Ahmed, Hoda Mostafa; Mahmoud, A. A.; Mahmoud, Mona F.; Ibrahim, Islam A.A.E.-H.

doi:10.1016/j.lfs.2021.120055

Cited by 7 publications

(5 citation statements)

References 54 publications

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“…Propranolol is a highly lipophilic non-selective β-blocker that can cross the blood brain barrier and can show weak β-arrestin agonistic effects [ 51 , 52 ]. Previously, propranolol has shown neuroprotective effect against retinal degeneration in a mouse model of light injury [ 19 ].…”

Section: Discussionmentioning

confidence: 99%

Adrenergic receptors blockade alleviates dexamethasone-induced neurotoxicity in adult male Wistar rats: Distinct effects on β-arrestin2 expression and molecular markers of neural injury

Mohamed,

Ahmad Ahmad,

Amin

et al. 2023

DARU J Pharm Sci

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Background Dexamethasone-induced neurotoxicity has been previously reported. However, the molecular mechanisms are still not completely understood. Objectives The current work aimed to investigate the modulatory effects of α- and β-adrenergic receptors on dexamethasone-induced neurotoxicity in rats focused on changes in β-arrestin2 and molecular markers of neural injury in cerebral cortex. Methods Male Wistar rats were subcutaneously injected with dexamethasone (10 mg/kg/day) for 7 days to induce neural injury in the cerebral cortex. The experiment involved 5 groups: control, dexamethasone, carvedilol, propranolol, and doxazosin. In the last 3 groups, drugs were given 2 hours before dexamethasone injection. At the end of experiment, brain samples were collected for measurement of brain derived neurotrophic factor (BDNF), glial fibrillary acidic protein (GFAP), kinase activity of protein kinase B (Akt), diacylglycerol (DAG), α-smooth muscle actin (α-SMA), Smad3, β-amyloid and phospho-tau protein levels in addition to histopathological examination of brain tissue using hematoxylin-eosin, Nissl, and Sirius red stains. Moreover, β-arrestin2 levels in the cerebral cortex were measured using immunohistochemical examination. Results Dexamethasone slightly reduced brain weight and significantly decreased BDNF, Akt kinase activity and β-arrestin2 but markedly induced degeneration of cortical neurons and significantly increased GFAP, DAG, α-SMA, Smad3, β-amyloid and phospho-tau protein levels compared to controls. Carvedilol, propranolol, and doxazosin reversed all dexamethasone-induced molecular changes and slightly ameliorated the histopathological changes. Carvedilol significantly increased brain weight and β-arrestin2 levels compared to dexamethasone, propranolol, and doxazosin groups. Conclusion blocking α- and/or β-adrenergic receptors alleviate dexamethasone-induced neurotoxicity despite their distinct effects on β-arrestin2 levels in the cerebral cortex. Graphical abstract

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Section: Discussionmentioning

confidence: 99%

Adrenergic receptors blockade alleviates dexamethasone-induced neurotoxicity in adult male Wistar rats: Distinct effects on β-arrestin2 expression and molecular markers of neural injury

Mohamed,

Ahmad Ahmad,

Amin

et al. 2023

DARU J Pharm Sci

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“… Propranolol and l-d- Isopropionic acid can reduce IR of HFrHFD mice by up-regulating β -inhibin 2 signaling activity. 505 Sarsasapogenin (ZGY) High-fat diet (HFD) C57BL/6 J mice; LPS-induced acute adipose tissue inflammation model ZGY treatment (80 mg/kg/d, ig, lasting for 18 days) can significantly inhibit the acute adipose tissue inflammation of LPS-treated mice. In obese mice fed with high-fat diet, taking ZGY orally (80 mg·kg/d for 6 weeks) can reduce the infiltration of macrophages, improve IRand reduce the inflammation of adipose tissue.…”

Section: The Diagnosis and Therapeutic Strategy Of Irmentioning

confidence: 99%

Trends in insulin resistance: insights into mechanisms and therapeutic strategy

Chi²,

Wang

et al. 2022

Sig Transduct Target Ther

243

132

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The centenary of insulin discovery represents an important opportunity to transform diabetes from a fatal diagnosis into a medically manageable chronic condition. Insulin is a key peptide hormone and mediates the systemic glucose metabolism in different tissues. Insulin resistance (IR) is a disordered biological response for insulin stimulation through the disruption of different molecular pathways in target tissues. Acquired conditions and genetic factors have been implicated in IR. Recent genetic and biochemical studies suggest that the dysregulated metabolic mediators released by adipose tissue including adipokines, cytokines, chemokines, excess lipids and toxic lipid metabolites promote IR in other tissues. IR is associated with several groups of abnormal syndromes that include obesity, diabetes, metabolic dysfunction-associated fatty liver disease (MAFLD), cardiovascular disease, polycystic ovary syndrome (PCOS), and other abnormalities. Although no medication is specifically approved to treat IR, we summarized the lifestyle changes and pharmacological medications that have been used as efficient intervention to improve insulin sensitivity. Ultimately, the systematic discussion of complex mechanism will help to identify potential new targets and treat the closely associated metabolic syndrome of IR.

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“…Propranolol, a beta-blocker, reduces myocardial contractility, autoregulation, conduction, and excitability. It also slows HR, diminishes cardiac output, and lowers myocardial oxygen consumption (Lin et al , 2020;Ibrahim et al , 2021;Peltenburg et al , 2022). The noradrenergic system plays a significant role in the consolidation of contextual fear memories (Fan et al , 2022), and propranolol is a widely studied drug for memory reconsolidation therapy in clinical settings.…”

Section: Treatment Ptsd From the Cardiovascular Systemmentioning

confidence: 99%

New recognition of heart-brain axis and its implication in the pathogenesis and treatment of PTSD

Li,

Zhang,

Ding

et al. 2024

Preprint

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Post-traumatic stress disorder (PTSD) is a complex psychological disorder provoked by distressing experiences, and it remains without highly effective intervention strategies. The exploration of PTSD’s underlying mechanisms is crucial for advancing diagnostic and therapeutic approaches. Current studies primarily explore PTSD through the lens of the CNS, investigating concrete molecular alterations in the cerebral area and neural circuit irregularities. However, the body’s response to external stressors, particularly the changes in cardiovascular function, is often pronounced, evidenced by notable cardiac dysfunction. Consequently, examining PTSD with a focus on cardiac function is vital for the early prevention and targeted management of the disorder. This review undertakes a comprehensive literature analysis to detail the alterations in brain and heart structures and functions associated with PTSD. It also synthesizes potential mechanisms of heart-brain axis interactions relevant to PTSD’s development. Ultimately, by considering cardiac function, this review proposes novel perspectives for PTSD’s prophylaxis and therapy.

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Propranolol and low-dose isoproterenol ameliorate insulin resistance, enhance β-arrestin2 signaling, and reduce cardiac remodeling in high-fructose, high-fat diet-fed mice: Comparative study with metformin

Cited by 7 publications

References 54 publications

Adrenergic receptors blockade alleviates dexamethasone-induced neurotoxicity in adult male Wistar rats: Distinct effects on β-arrestin2 expression and molecular markers of neural injury

Adrenergic receptors blockade alleviates dexamethasone-induced neurotoxicity in adult male Wistar rats: Distinct effects on β-arrestin2 expression and molecular markers of neural injury

Trends in insulin resistance: insights into mechanisms and therapeutic strategy

New recognition of heart-brain axis and its implication in the pathogenesis and treatment of PTSD

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