Fucoxanthin protects neonatal rat cardiomyocytes and attenuates high glucose-mediated oxidative stress via the AMPK pathway
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Department of Pediatrics, Jiangsu Taizhou People’s Hospital, Taizhou City, Jiangsu Province, China
Department of Neonatology, Wuhan Children’s Hospital (Wuhan Maternal and Child Healthcare Hospital), Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China
Submission date: 2019-10-10
Final revision date: 2020-01-31
Acceptance date: 2020-02-15
Online publication date: 2020-04-15
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, Iry neonatal rat cardiomyocytes were cultured in a high glucose environment (30 mM/l) in the presence and absence of FXN. Apoptosis, cell viability, activity of NADPH oxidase and expression level of its subunits, levels of MDA and activity of endogenous antioxidant enzymes were studied. We also confirmed the involved pathway by studying the expression of AMPK, GSK-3 and Akt in the cardiomyocytes.

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.

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.