Diphlorethohydroxycarmalol Attenuates Methylglyoxal-Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

Oxidative Medicine and Cellular Longevity
Seon-Heui ChaHee-Sook Jun

Abstract

Diabetic nephropathy is the leading cause of end-stage renal disease in patients with diabetes mellitus. Oxidative stress has been shown to play an important role in pathogeneses of renal damage in diabetic patients. Here, we investigated the protective effect of diphlorethohydroxycarmalol (DPHC), which is a polyphenol isolated from an edible seaweed, Ishige okamurae, on methylglyoxal-induced oxidative stress in HEK cells, a human embryonic kidney cell line. DPHC treatment inhibited methylglyoxal- (MGO-) induced cytotoxicity and ROS production. DPHC activated the Nrf2 transcription factor and increased the mRNA expression of antioxidant and detoxification enzymes, consequently reducing MGO-induced advanced glycation end product formation. In addition, DPHC increased glyoxalase-1 mRNA expression and attenuated MGO-induced advanced glycation end product formation in HEK cells. These results suggest that DPHC possesses a protective activity against MGO-induced cytotoxicity in human kidney cells by preventing oxidative stress and advanced glycation end product formation. Therefore, it could be used as a potential therapeutic agent for the prevention of diabetic nephropathy.

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Citations

Aug 1, 2018·Marine Drugs·Manuel Gómez-GuzmánJulio Gálvez
Jan 19, 2021·Archives of Physiology and Biochemistry·Shahnaz MojadamiLayasadat Khorsandi
Jan 6, 2021·International Journal of Molecular Sciences·Silvia YumnamSun Yeou Kim
Jul 4, 2021·Biomedicine & Pharmacotherapy = Biomédecine & Pharmacothérapie·Nada H EisaEman Said

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Methods Mentioned

BETA
electron spin resonance
ESR
PCR
protein assay
flow cytometry
Assay
confocal microscopy

Software Mentioned

FlowJo
ImageJ

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