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Published on: July 13, 2018
Astaxanthin protects mesangial cells from hyperglycemia-induced oxidative signaling
Emiko Manabe1, Osamu Handa, Yuji Naito
1School of Nursing, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.
Abstract:
Astaxanthin (ASX) is a carotenoid that has potent protective effects on diabetic nephropathy in mice model of type 2 diabetes. In this study, we investigated the protective mechanism of ASX on the progression of diabetic nephropathy using an in vitro model of hyperglycemia, focusing on mesangial cells. Normal human mesangial cells (NHMCs) were cultured in the medium containing normal (5 mM) or high (25 mM) concentrations of D-glucose. Reactive oxygen species (ROS) production, the activation of nuclear transcription factors such as nuclear factor kappa B (NFkappaB) and activator protein-1 (AP-1), and the expression/production of transforming growth factor-beta 1 (TGFbeta(1)) and monocyte chemoattractant protein-1 (MCP-1) were evaluated in the presence or absence of ASX. High glucose (HG) exposure induced significant ROS production in mitochondria of NHMCs, which resulted in the activation of transcription factors, and subsequent expression/production of cytokines that plays an important role in the mesangial expansion, an important event in the pathogenesis of diabetic nephropathy. ASX significantly suppressed HG-induced ROS production, the activation of transcription factors, and cytokine expression/production by NHMCs. In addition, ASX accumulated in the mitochondria of NHMCs and reduced the production of ROS-modified proteins in mitochondria. ASX may prevent the progression of diabetic nephropathy mainly through ROS scavenging effect in mitochondria of mesangial cells and thus is expected to be very useful for the prevention of diabetic nephropathy.
Insights
Astaxanthin (ASX) protects against diabetic nephropathy by reducing mitochondrial reactive oxygen species (ROS) in kidney cells. This carotenoid inhibits key inflammatory pathways, offering a potential preventative strategy for diabetic kidney disease.
Area of Science:
- Nephrology
- Cell Biology
- Biochemistry
Background:
- Diabetic nephropathy is a major complication of diabetes, characterized by kidney damage.
- High glucose levels induce oxidative stress and inflammation in kidney mesangial cells, contributing to disease progression.
Purpose of the Study:
- To investigate the protective mechanism of astaxanthin (ASX) against high glucose-induced damage in normal human mesangial cells (NHMCs).
- To elucidate the role of reactive oxygen species (ROS) and inflammatory pathways in ASX's protective effects.
Main Methods:
- NHMCs were cultured under normal or high glucose conditions with or without ASX.
- Assessed ROS production, mitochondrial ROS, transcription factor activation (NF-κB, AP-1), and expression of TGF-β1 and MCP-1.
Main Results:
- High glucose significantly increased ROS production, mitochondrial ROS, transcription factor activation, and cytokine expression in NHMCs.
- ASX markedly suppressed high glucose-induced ROS production, particularly in mitochondria.
- ASX inhibited the activation of NF-κB and AP-1 and reduced the expression of TGF-β1 and MCP-1.
Conclusions:
- Astaxanthin exerts protective effects against diabetic nephropathy by scavenging mitochondrial ROS in mesangial cells.
- ASX mitigates high glucose-induced inflammation and cellular damage, suggesting its therapeutic potential for preventing diabetic kidney disease.
