Um Novo Sistema de Prognóstico para Implantes Dentários

Najafi, Babak; Kheirieh, Parisa; Cappetta, Emil G; Najafi, Ahmad; Singh, Saurabh

doi:10.20432/prd607

Cited by 1 publication

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“…Accumulating evidence has shown that melatonin regulates physiological responses, such as sleep, circadian rhythms, immune defense, and neuroendocrine actions [7,9]. Melatonin (N-acetyl-5methoxytryptamine) is also a pleiotropic and multifunctioning indoleamine, which plays roles in antioxidative, antitumor, immunoregulatory activities [10]. Thus, melatonin has been reported to modulate a wide spectrum of molecular pathways, including apoptosis, autophagy, oxidative stress, inflammation, cellular injury, and fibrosis [11][12][13][14].…”

Section: Ivyspringmentioning

confidence: 99%

Melatonin Protects Human Renal Proximal Tubule Epithelial Cells Against High Glucose-Mediated Fibrosis via the Cellular Prion Protein-TGF-β-Smad Signaling Axis

Han¹,

Yoon²,

Go³

et al. 2020

Int. J. Med. Sci.

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Diabetes-mediated hyperglycemia is a major risk factor for renal fibrosis, resulting in the development of chronic kidney diseases. To address this issue, the effect of melatonin, which has an antioxidative potential, on renal fibrosis in human renal proximal tubule epithelial cells under high glucose conditions was investigated. Under high glucose conditions, the generation of reactive oxygen species was drastically increased in human renal proximal tubule epithelial cells, which lead to the inhibition of cell proliferation, enlargement of cell size, reduction of cell survival, and suppression of antioxidant enzyme activities. High glucose also increased the expression of transforming growth factor-β, leading to an increase in Smad2 phosphorylation. These fibrotic phenotype changes increased the expression of fibrosis-mediated extracellular matrix proteins, such as fibronectin, collagen I, and α-smooth muscle actin. In addition, the level of cellular prion protein (PrP C), which is associated with several biological processes, was decreased by exposure to high glucose conditions. Melatonin recovered the expression levels of PrP C under high glucose conditions via phosphorylation of Akt, resulting in the prevention of high glucose-induced fibrosis. In particular, overexpression of PrP C blocked the high glucose-mediated fibrotic phenotype change. These findings indicate that melatonin could be a powerful agent for treating hyperglycemia-induced renal fibrosis.

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Section: Ivyspringmentioning

confidence: 99%