Ethyl Pyruvate Prevents Methyglyoxal-Induced Retinal Vascular Injury in Rats

Kim, Jung-Hyun; Lee, Yun Mi; Kim, Chan-Sik; Sohn, Eunjin; Jo, Kyuhyung; Shin, So Dam; Kim, Jin Sook

doi:10.1155/2013/460820

Cited by 8 publications

(8 citation statements)

References 46 publications

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“…VEGF directly decreases the EC tight junction (TJ) content or increases their phosphorylation ( 7 ), either or the two of these effects may enhance paracellular permeability. In support of this, a previous study by our group has demonstrated that methylglyoxal, a potent precursor of AGEs, increased the expression of VEGF in retinal tissues, which elicits retinal vascular hyperpermeability ( 8 ).…”

Section: Introductionsupporting

confidence: 59%

OSSC1E-K19, a novel phytochemical component of Osteomeles schwerinae, prevents glycated albumin-induced retinal vascular injury in rats

Kim

et al. 2015

Molecular Medicine Reports

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In the pathophysiology of diabetic retinopathy (DR), advanced glycation end products (AGEs) and vascular endothelial growth factor (VEGF) are thought to have important roles. It is known that VEGF causes a breakdown of the blood-retinal barrier (BRB) and retinal neovascularization; however, how AGEs affect the retina has largely remained elusive. OSSC1E-K19 is a novel phytochemical component of Osteomeles schwerinae. The objective of the present study was to evaluate the protective effects of OSSC1E-K19 on retinal vascular injury in AGE-modified rat serum albumin (AGE-RSA)-induced retinopathy. AGE-RSA-injected rat eyes were used investigate the protective effects of OSSC1E-K19 on BRB breakdown. Intravitreal injection of OSSC1E-K19 prevented AGE-RSA-induced BRB breakdown and decreased retinal VEGF expression in retinal vessels. In addition, OSSC1E-K19 inhibited the loss of occludin, a significant tight junction protein. These results supported the potential therapeutic utility of OSSC1E-K19 for retinal vascular permeability diseases.

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Section: Introductionsupporting

confidence: 59%

OSSC1E-K19, a novel phytochemical component of Osteomeles schwerinae, prevents glycated albumin-induced retinal vascular injury in rats

Kim

et al. 2015

Molecular Medicine Reports

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“…Pyruvate showed anti-inflammatory effects in various animal models but was restricted by its low stability in aqueous solutions [ 102 ]. Therefore, EP constitutes a more stable compound than pyruvate and exerts anti-inflammatory and protective effects in ROS-mediated models of ischemia and reperfusion [ 103 , 104 , 105 ], hemorrhagic shock [ 106 ], septic shock [ 107 , 108 ], cecal ligation and perforation [ 109 ], acute renal failure [ 110 , 111 ], pancreatitis [ 112 , 113 , 114 , 115 ], thermal injury [ 116 ], brain injury [ 117 , 118 , 119 , 120 , 121 ], cardiac injury [ 122 , 123 ], retinal damage, and uveitis and cataract [ 124 , 125 , 126 , 127 , 128 , 129 ]. The effects of EP on RAGE were also analyzed in several studies, showing a reduction of RAGE expression upon EP treatment [ 130 , 131 ].…”

Section: Glo-i Ages and Rage In Chronic Liver Injurymentioning

confidence: 99%

The Role of Glyoxalase-I (Glo-I), Advanced Glycation Endproducts (AGEs), and Their Receptor (RAGE) in Chronic Liver Disease and Hepatocellular Carcinoma (HCC)

Hollenbach¹

2017

IJMS

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Glyoxalase-I (Glo-I) and glyoxalase-II (Glo-II) comprise the glyoxalase system and are responsible for the detoxification of methylglyoxal (MGO). MGO is formed non-enzymatically as a by-product, mainly in glycolysis, and leads to the formation of advanced glycation endproducts (AGEs). AGEs bind to their receptor, RAGE, and activate intracellular transcription factors, resulting in the production of pro-inflammatory cytokines, oxidative stress, and inflammation. This review will focus on the implication of the Glo-I/AGE/RAGE system in liver injury and hepatocellular carcinoma (HCC). AGEs and RAGE are upregulated in liver fibrosis, and the silencing of RAGE reduced collagen deposition and the tumor growth of HCC. Nevertheless, data relating to Glo-I in fibrosis and cirrhosis are preliminary. Glo-I expression was found to be reduced in early and advanced cirrhosis with a subsequent increase of MGO-levels. On the other hand, pharmacological modulation of Glo-I resulted in the reduced activation of hepatic stellate cells and therefore reduced fibrosis in the CCl4-model of cirrhosis. Thus, current research highlighted the Glo-I/AGE/RAGE system as an interesting therapeutic target in chronic liver diseases. These findings need further elucidation in preclinical and clinical studies.

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“…Such compounds were found to prevent from protein glycation by scavenging MG and, some of them, by activating GLO1. Other molecules discovered to have MG‐scavenging properties include the polysaccharides, prebiotics, chitosan, the anti‐inflammatory molecule ethyl piruvate . From this group of compounds, the isoflavone genistein has been recently suggested to be particularly effective in preventing MG‐induced glycation .…”

Section: The Promise Of New Therapeutic Targetsmentioning

confidence: 99%

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

Matafome

Rodrigues

Sena

et al. 2016

Medicinal Research Reviews

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Glucose and fructose metabolism originates the highly reactive byproduct methylglyoxal (MG), which is a strong precursor of advanced glycation end products (AGE). The MG has been implicated in classical diabetic complications such as retinopathy, nephropathy, and neuropathy, but has also been recently associated with cardiovascular diseases and central nervous system disorders such as cerebrovascular diseases and dementia. Recent studies even suggested its involvement in insulin resistance and beta-cell dysfunction, contributing to the early development of type 2 diabetes and creating a vicious circle between glycation and hyperglycemia. Despite several drugs and natural compounds have been identified in the last years in order to scavenge MG and inhibit AGE formation, we are still far from having an effective strategy to prevent MG-induced mechanisms. This review summarizes the endogenous and exogenous sources of MG, also addressing the current controversy about the importance of exogenous MG sources. The mechanisms by which MG changes cell behavior and its involvement in type 2 diabetes development and complications and the pathophysiological implication are also summarized. Particular emphasis will be given to pathophysiological relevance of studies using higher MG doses, which may have produced biased results. Finally, we also overview the current knowledge about detoxification strategies, including modulation of endogenous enzymatic systems and exogenous compounds able to inhibit MG effects on biological systems.

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Ethyl Pyruvate Prevents Methyglyoxal-Induced Retinal Vascular Injury in Rats

Cited by 8 publications

References 46 publications

OSSC1E-K19, a novel phytochemical component of Osteomeles schwerinae, prevents glycated albumin-induced retinal vascular injury in rats

OSSC1E-K19, a novel phytochemical component of Osteomeles schwerinae, prevents glycated albumin-induced retinal vascular injury in rats

The Role of Glyoxalase-I (Glo-I), Advanced Glycation Endproducts (AGEs), and Their Receptor (RAGE) in Chronic Liver Disease and Hepatocellular Carcinoma (HCC)

Methylglyoxal in Metabolic Disorders: Facts, Myths, and Promises

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