Diphlorethohydroxycarmalol Attenuates Methylglyoxal-Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells.
Seon-Heui ChaYongha HwangSoo-Jin HeoYoon Sin OhPublished in: Oxidative medicine and cellular longevity (2018)
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.
Keyphrases
- induced apoptosis
- oxidative stress
- diabetic rats
- diabetic nephropathy
- endothelial cells
- high glucose
- cell cycle arrest
- endoplasmic reticulum stress
- transcription factor
- dna damage
- cell death
- signaling pathway
- type diabetes
- induced pluripotent stem cells
- end stage renal disease
- drug induced
- ischemia reperfusion injury
- skeletal muscle
- metabolic syndrome
- hydrogen peroxide
- cell proliferation
- mass spectrometry
- pluripotent stem cells
- pi k akt
- glycemic control
- atomic force microscopy