Long-term administration of advanced glycation end-product stimulates the activation of NLRP3 inflammasome and sparking the development of renal injury

Yeh, Wan Ju; Yang, Hsin Yi; Pai, Man Hui; Wu, Chi Hao; Chen, Jiun Rong

doi:10.1016/j.jnutbio.2016.09.014

Cited by 43 publications

(34 citation statements)

References 51 publications

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“…Additionally, Shahzad et al (2016) Zhou, Wang, Zhu, & Hao, 2012). Furthermore, high AGEs burden stimulated the activation of NLRP3 inflammasome and sparked the development of renal injury in mice (Yeh, Yang, Pai, Wu, & Chen, 2017). In our results, Sar could significantly decrease AGEs levels and reversed the elevation of RAGE expression accompanied by NLRP3 inflammasome suppression in the renal cortex of diabetic rats.…”

Section: Discussionsupporting

confidence: 50%

“…Accumulation of AGEs and subsequent enhanced interaction with their receptor RAGE are the common pathological processes of diabetic complications, including DN (Kumar Pasupulati, Chitra, & Reddy, ; Zhou, Wang, Zhu, & Hao, ). Furthermore, high AGEs burden stimulated the activation of NLRP3 inflammasome and sparked the development of renal injury in mice (Yeh, Yang, Pai, Wu, & Chen, ). In our results, Sar could significantly decrease AGEs levels and reversed the elevation of RAGE expression accompanied by NLRP3 inflammasome suppression in the renal cortex of diabetic rats.…”

Section: Discussionmentioning

confidence: 99%

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Protective effects of sarsasapogenin against early stage of diabetic nephropathy in rats

Liu

Hao

Chen

et al. 2018

Phytotherapy Research

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Rhizome of Anemarrhena asphodeloides Bunge (AA, family Liliaceae) has been widely used in China for thousands of years to treat febrile diseases and diabetes. Steroidal saponins from AA show good antidiabetes effects and ameliorate diabetic complications. This study was designed to investigate the effects of sarsasapogenin (Sar), a major sapogenin from AA, on diabetic nephropathy (DN) in rats, and to explore the possible mechanisms. Diabetic rats were divided into 3 groups treated orally with Sar (0, 20, or 60 mg/kg) and carboxymethylcellulose sodium, whereas normal rats for Sar (0 or 60 mg/kg) and carboxymethylcellulose sodium. We found that chronic treatment with Sar for 9 weeks significantly ameliorated renal dysfunction of diabetic rats, as evidenced by decreases in albuminuria, kidney weight index, serum uric acid, and morphologic changes such as extracellular matrix expansion and accumulation (fibronectin and collagen IV levels, etc.). Meanwhile, Sar treatment resulted in decreases in interleukin-18, NLRP3, and activated caspase 1 levels as well as advanced glycation endproducts (AGEs) and their receptor (RAGE) levels in the renal cortex of diabetic rats. However, Sar has no effects on the above indices in the normal rats. Therefore, Sar can markedly ameliorate diabetic nephropathy in rats via inhibition of NLRP3 inflammasome activation and AGEs-RAGE interaction.

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Section: Discussionsupporting

confidence: 50%

Section: Discussionmentioning

confidence: 99%

Protective effects of sarsasapogenin against early stage of diabetic nephropathy in rats

Liu

Hao

Chen

et al. 2018

Phytotherapy Research

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“…The inflammasomes are multiporotein platforms activated by interaction of a variety of danger signals with membrane and cytoplasmic receptors. Among these receptors, a role for two AGE receptors, namely RAGE and Galectin-3, in inflammasome activation has been proposed [79,80,81,82]. However, there is still contrasting data about the exact mechanisms by which both Galectin-3 and RAGE act on inflammasome assembling.…”

Section: Dietary Sugar-induced Glycation: Interference On Cell Funmentioning

confidence: 99%

Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

2017

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The rapid increase in metabolic diseases, which occurred in the last three decades in both industrialized and developing countries, has been related to the rise in sugar-added foods and sweetened beverages consumption. An emerging topic in the pathogenesis of metabolic diseases related to modern nutrition is the role of Advanced Glycation Endproducts (AGEs). AGEs can be ingested with high temperature processed foods, but also endogenously formed as a consequence of a high dietary sugar intake. Animal models of high sugar consumption, in particular fructose, have reported AGE accumulation in different tissues in association with peripheral insulin resistance and lipid metabolism alterations. The in vitro observation that fructose is one of the most rapid and effective glycating agents when compared to other sugars has prompted the investigation of the in vivo fructose-induced glycation. In particular, the widespread employment of fructose as sweetener has been ascribed by many experimental and observational studies for the enhancement of lipogenesis and intracellular lipid deposition. Indeed, diet-derived AGEs have been demonstrated to interfere with many cell functions such as lipid synthesis, inflammation, antioxidant defences, and mitochondrial metabolism. Moreover, emerging evidence also in humans suggest that this impact of dietary AGEs on different signalling pathways can contribute to the onset of organ damage in liver, skeletal and cardiac muscle, and the brain, affecting not only metabolic control, but global health. Indeed, the most recent reports on the effects of high sugar consumption and diet-derived AGEs on human health reviewed here suggest the need to limit the dietary sources of AGEs, including added sugars, to prevent the development of metabolic diseases and related comorbidities.

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“…Yeh et al . reported that AGEs activated NLRP3 inflammasome, up‐regulated the expression of the pro‐inflammatory cytokine IL‐1 β and led to endothelial cell dysfunction . Our results implied that NLRP3 inflammasome could be activated by AGEs‐induced ROS, ultimately led to increased mRNA expression of IL‐1 β and IL‐18, but this trend was reversed by CA.…”

Section: Resultsmentioning

confidence: 59%

Caffeic Acid Inhibits the Formation of Advanced Glycation End Products (AGEs) and Mitigates the AGEs‐Induced Oxidative Stress and Inflammation Reaction in Human Umbilical Vein Endothelial Cells (HUVECs)

Cao

Xia

Zeng

et al. 2019

Chemistry & Biodiversity

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The advanced glycation end products (AGEs) are the compounds produced by non‐enzymatic glycation reaction of proteins and sugars, which can induce the generation of free radicals and the expression of inflammatory factors, thereby playing an important role in vascular dysfunction in diabetes. To investigate the effects of caffeic acid (CA) on glycation formed by glucose and protein, various spectroscopic techniques and molecular docking methods were carried out. Furthermore, the protective effects of CA on human umbilical vein endothelial cells (HUVECs) damaged by AGEs were detected. The results indicated that CA inhibited AGEs formation in vitro, decreased the expression of IL‐1β, IL‐18, ICAM‐1, VCAM‐1, NLRP3, Caspase‐1 and CRP (C‐reactive protein) and reduced the ROS in HUVECs exposed to AGEs. Our findings suggested that the supplementation with dietary CA could prevent and delay the AGEs‐induced vascular dysfunction in diabetes.

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Long-term administration of advanced glycation end-product stimulates the activation of NLRP3 inflammasome and sparking the development of renal injury

Cited by 43 publications

References 51 publications

Protective effects of sarsasapogenin against early stage of diabetic nephropathy in rats

Protective effects of sarsasapogenin against early stage of diabetic nephropathy in rats

Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease

Caffeic Acid Inhibits the Formation of Advanced Glycation End Products (AGEs) and Mitigates the AGEs‐Induced Oxidative Stress and Inflammation Reaction in Human Umbilical Vein Endothelial Cells (HUVECs)

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