Astaxanthin protects mesangial cells from hyperglycemia‐induced oxidative signaling
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 (NFκB) and activator protein‐1 (AP‐1), and the expression/production of transforming growth factor‐beta 1 (TGFβ 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. J. Cell. Biochem. 103: 1925–1937, 2007. © 2007 Wiley‐Liss, Inc.
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High glucose increased ROS fluorescence in human mesangial cells associated with potentially harmful cytokine expression.
“Manabe et al. (208) reported that high glucose increased ROS fluorescence in human mesangial cells associated with potentially harmful cytokine expression, an effect that was blocked by astaxanthin, a carotenoid that accumulated in mitochondria.”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [208]
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- Authors
- Manabe, E., Handa, O., Naito, Y., Mizushima, K., Akagiri, S., Adachi, S., Takagi, T., Kokura, S., Maoka, T., & Yoshikawa, T.
- Affiliations
- Kyoto Prefectural University of Medicine (JP)
- Research Institute for Production Development (JP)
- Corresponding author
- Naito, Yuji
- Venue
- Journal of Cellular Biochemistry
- Publisher
- Wiley
- Published
- 2007-10-22
- Volume
- 103
- Issue
- 6
- Pages
- 1925-1937
- ISSN
- 0730-2312 (ISSN-L)
- 1097-4644
- OpenAlex
- W1979613828
- Cited by
- 132
- References
- 50
- Citations by year
- 2026: 2 · 2025: 9 · 2024: 2 · 2023: 9 · 2022: 8 · 2021: 12 · 2020: 10 · 2019: 3 · 2018: 7 · 2017: 8 · 2016: 7 · 2015: 3 · 2014: 8 · 2013: 7 · 2012: 9
- FWCI
- 5.33
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Cellular Biochemistry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Keywords
- astaxanthin, diabetic nephropathy, mesangial cells, hyperglycemia, reactive oxygen species, mitochondrial reactive oxygen species, NF-κB, AP-1, TGF-β1, MCP-1, mesangial expansion, carotenoids, oxidative stress
- MeSH terms
- Cell Line, Diabetic Neuropathies, Humans, Hyperglycemia, Mitochondria, Oxidation-Reduction, Signal Transduction, NF-kappa B, Reactive Oxygen Species, Transcription Factor AP-1, Chemokine CCL2, Mitogen-Activated Protein Kinases, Xanthophylls, Mesangial Cells, Transforming Growth Factor beta1
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