ArticleArchives of medical science : AMS2025
Fucoxanthin protects neonatal rat cardiomyocytes and attenuates high glucose-mediated oxidative stress via the AMPK pathway.
Article in Archives of medical science : AMS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Advances in natural compounds modulating autophagy for the therapeutic intervention of heart failure.Molecular and cellular biochemistry · 2026Review
- HMGCS2 silencing attenuates high glucose-induced in vitro diabetic cardiomyopathy by increasing cell viability, and inhibiting apoptosis, inflammation, and oxidative stress.Bioengineered · 2022Article
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2 authors.
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Abstract
Introduction: Diabetic cardiomyopathy (DC) is associated with impaired diastolic function. Hyperglycemia-mediated oxidative stress and apoptosis are the major factors responsible for DC. Also NADPH oxidase is the main source of ROS in cardiac cells or cardiomyocytes. Here we evaluated the effect of fucoxanthin (FXN) on high glucose cultured neonatal rat cardiomyocytes. Material and methods: For the study, I Results: The high glucose environment increased the production of ROS, and FXN decreased the oxidative burden by inhibiting ROS in cultured neonatal rat cardiomyocytes. FXN inhibited the activity of NADPH oxidase and Rac1 also increased the expression of its subunits. Treatment of FXN reversed the MDA, CAT, GSHpx, SOD activity and GSH contents. FXN down-regulated the levels of Bax and up-regulated the levels of Bcl-2 (anti-apoptotic protein); treatment protected the cardiomyocytes from injury. Also, FXN increased the levels of pAMPK in cardiac cells treated with high glucose. The pharmacological inhibitor of AMPK abolished the activities of FXN in high glucose induced cardiomyocytes. Conclusions: FXN exerted protective action on cardiac cells subjected to high glucose-mediated apoptosis by suppressing NADPH oxidase-mediated production of ROS and maintaining the antioxidant defense in the tissues. The attenuating activity of FXN was propagated via the AMPK cascade.
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