Neuropeptide α-Melanocyte-Stimulating Hormone Promotes Neurological Recovery and Repairs Cerebral Ischemia/Reperfusion Injury in Type 1 Diabetes

Goit, Rajesh Kumar; Ng, Tsz Chung; Tam, Ka Cheung; Tsang, Jessica Oi-Ling; Taylor, Andrew W.; Lo, Amy Cheuk Yin

doi:10.1007/s11064-021-03453-4

Cited by 4 publications

(9 citation statements)

References 72 publications

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“…Fifty microgram/mouse of α-MSH had been shown to be neuroprotective in cerebral I/R injury (Goit et al, 2021). It also yielded beneficial effects in recovering b-wave amplitude and OPs in ERG measurements as describe above.…”

Section: α-Melanocyte-stimulating Hormone Preserved Retinal Structure...mentioning

confidence: 90%

“…Retinal I/R injury was achieved by blocking blood flow into the middle cerebral artery (MCA) as previously described (Lo et al, 2005(Lo et al, , 2007Li et al, 2009Li et al, , 2011Li et al, , 2012Goit et al, 2021). Briefly, animals were anesthetized with 2% isoflurane in 70% N 2 O and 30% O 2 for induction and 1-1.5% isoflurane in 70% N 2 O and 30% O 2 for maintenance during surgery.…”

Section: Animal Model Of Retinal Ischemia and Reperfusionmentioning

confidence: 99%

“…The shamoperated animals underwent MCA exposure without occlusion. The core temperature during the surgery was maintained approximately at 37 • C using a heating pad as described (Goit et al, 2021).…”

Section: Animal Model Of Retinal Ischemia and Reperfusionmentioning

confidence: 99%

“…Animals were injected with 2, 10, 20, 50, 70, or 100 µg/mouse of α-MSH (Bachem AG, Switzerland) in phosphate-buffer saline (PBS) intraperitoneally at 1 h after ischemia and 1 h after reperfusion. Since α-MSH at 50 µg/mouse showed neuroprotective effects in cerebral I/R injury (Goit et al, 2021), this dosage was later used to further evaluate its protective effects in the I/R induced retinal damage. PBS was injected as a vehicle.…”

Section: α-Melanocyte-stimulating Hormone Treatmentmentioning

confidence: 99%

“…Mainly synthesized in the hypothalamus and the brain stem as well as in the pituitary gland, POMC-derived peptides have a wide range of actions such as energy homeostasis, steroidogenesis, pigmentation, thermoregulation, and anti-inflammation. Several studies showed that α-MSH has protective effects against ischemia/reperfusion (I/R) organ damages such as brain (Huh et al, 1997;Huang and Tatro, 2002;Aronsson et al, 2006;Chen et al, 2008;Savos et al, 2011;Goit et al, 2021), eye (Varga et al, 2013), heart (Vecsernyes et al, 2003), kidney (Chiao et al, 1997;Gong et al, 2004), and gut (Hassoun et al, 2002;Zou et al, 2003). Indeed, α-MSH counteracts retinal degeneration during early diabetes, and it alleviates the pro-inflammatory microenvironment caused by hyperglycemia in diabetic retina (Cai et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

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Anti-inflammatory α-Melanocyte-Stimulating Hormone Protects Retina After Ischemia/Reperfusion Injury in Type I Diabetes

Goit

Taylor

2022

Front. Neurosci.

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Retinal ischemia/reperfusion (I/R) injury is a major cause of vision loss in many ocular diseases. Retinal I/R injury is common in diabetic retinopathy, which as a result of hyperglycemia damages the retina and can cause blindness if left untreated. Inflammation is a major contributing factor in the pathogenesis of I/R injury. α-Melanocyte-stimulating hormone (α-MSH) is an anti-inflammatory peptide hormone that has displayed protective effects against I/R-induced organ damages. Here, we aimed to investigate the protective role of α-MSH on I/R-induced diabetic retinal damage using hyperglycemic C57BL/6J Ins2Akita/+ mice. Experimental I/R injury was induced by blocking the right middle cerebral artery (MCA) for 2 h followed by 2 h or 22 h of reperfusion using the intraluminal method. Since ophthalmic artery originates proximal to the origin of the MCA, the filament also blocked blood supply to the retina. Upon treatment with α-MSH at 1 h after ischemia and 1 h after reperfusion, animals displayed significant improvement in amplitudes of b-wave and oscillatory potentials during electroretinography. α-MSH also prevented I/R-induced histological alterations and inhibited the development of retinal swelling. Loss of retinal ganglion cells as well as oxidative stress were significantly attenuated in the α-MSH-treated retinae. Level of interleukin 10 was significantly increased after α-MSH treatment. Moreover, gene expression of glutamate aspartate transporter 1, monocarboxylate transporter (MCT) 1 and MCT-2 were significantly higher after α-MSH administration. In conclusion, α-MSH mitigates the severity of I/R-induced retinal damage under hyperglycemic condition. These beneficial effects of α-MSH may have important therapeutic implications against retinal I/R injury under hyperglycemic condition.

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Section: α-Melanocyte-stimulating Hormone Preserved Retinal Structure...mentioning

confidence: 90%

Section: Animal Model Of Retinal Ischemia and Reperfusionmentioning

confidence: 99%

Section: Animal Model Of Retinal Ischemia and Reperfusionmentioning

confidence: 99%

Section: α-Melanocyte-stimulating Hormone Treatmentmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Anti-inflammatory α-Melanocyte-Stimulating Hormone Protects Retina After Ischemia/Reperfusion Injury in Type I Diabetes

Goit

Taylor

2022

Front. Neurosci.

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A comparative study on the effects of human serum albumin and α-melanocyte-stimulating hormone fusion proteins on the anti-neuroinflammatory in the central nervous system of adult mice

Liu,

Li,

Wei

et al. 2024

Neuropeptides

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Cognitive dysfunction in diabetes: abnormal glucose metabolic regulation in the brain

Zhang

Wen

et al. 2023

Front. Endocrinol.

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Cognitive dysfunction is increasingly recognized as a complication and comorbidity of diabetes, supported by evidence of abnormal brain structure and function. Although few mechanistic metabolic studies have shown clear pathophysiological links between diabetes and cognitive dysfunction, there are several plausible ways in which this connection may occur. Since, brain functions require a constant supply of glucose as an energy source, the brain may be more susceptible to abnormalities in glucose metabolism. Glucose metabolic abnormalities under diabetic conditions may play an important role in cognitive dysfunction by affecting glucose transport and reducing glucose metabolism. These changes, along with oxidative stress, inflammation, mitochondrial dysfunction, and other factors, can affect synaptic transmission, neural plasticity, and ultimately lead to impaired neuronal and cognitive function. Insulin signal triggers intracellular signal transduction that regulates glucose transport and metabolism. Insulin resistance, one hallmark of diabetes, has also been linked with impaired cerebral glucose metabolism in the brain. In this review, we conclude that glucose metabolic abnormalities play a critical role in the pathophysiological alterations underlying diabetic cognitive dysfunction (DCD), which is associated with multiple pathogenic factors such as oxidative stress, mitochondrial dysfunction, inflammation, and others. Brain insulin resistance is highly emphasized and characterized as an important pathogenic mechanism in the DCD.

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Neuropeptide α-Melanocyte-Stimulating Hormone Promotes Neurological Recovery and Repairs Cerebral Ischemia/Reperfusion Injury in Type 1 Diabetes

Cited by 4 publications

References 72 publications

Anti-inflammatory α-Melanocyte-Stimulating Hormone Protects Retina After Ischemia/Reperfusion Injury in Type I Diabetes

Anti-inflammatory α-Melanocyte-Stimulating Hormone Protects Retina After Ischemia/Reperfusion Injury in Type I Diabetes

A comparative study on the effects of human serum albumin and α-melanocyte-stimulating hormone fusion proteins on the anti-neuroinflammatory in the central nervous system of adult mice

Cognitive dysfunction in diabetes: abnormal glucose metabolic regulation in the brain

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