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Isolation and Cryopreservation of Neonatal Rat Cardiomyocytes
Published on: April 9, 2015
Fucoxanthin protects neonatal rat cardiomyocytes and attenuates high glucose-mediated oxidative stress via the AMPK
1Department of Pediatrics, Jiangsu Taizhou People's Hospital, Taizhou City, Jiangsu Province, China.
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, 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-3β and Akt in the cardiomyocytes.
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.
Insights
Fucoxanthin (FXN) protects heart cells from high glucose damage by reducing oxidative stress and apoptosis. This protective effect is mediated through the AMPK pathway, highlighting FXN
Area of Science:
- Cardiovascular Biology
- Oxidative Stress Research
- Pharmacology
Background:
- Diabetic cardiomyopathy (DC) is characterized by impaired diastolic function, primarily driven by hyperglycemia-induced oxidative stress and apoptosis.
- NADPH oxidase is identified as a key source of reactive oxygen species (ROS) in cardiomyocytes, contributing to DC pathogenesis.
- Fucoxanthin (FXN), a marine carotenoid, is investigated for its potential therapeutic effects in managing cellular damage.
Purpose of the Study:
- To evaluate the protective effects of fucoxanthin (FXN) on neonatal rat cardiomyocytes cultured under high glucose conditions.
- To investigate the impact of FXN on oxidative stress markers, apoptosis, and the underlying molecular pathways in cardiomyocytes.
- To determine the role of the AMPK signaling pathway in mediating the cardioprotective effects of FXN.
Main Methods:
- Neonatal rat cardiomyocytes were cultured in high glucose (30 mM/l) with and without FXN.
- Assessed apoptosis, cell viability, NADPH oxidase activity and subunit expression, MDA levels, and antioxidant enzyme activities (CAT, GSHpx, SOD).
- Examined the expression of key signaling molecules including AMPK, GSK-3β, and Akt to elucidate the involved pathway.
Main Results:
- High glucose increased ROS production; FXN significantly reduced oxidative burden by inhibiting ROS and NADPH oxidase activity.
- FXN treatment reversed hyperglycemia-induced increases in MDA and restored antioxidant enzyme activities and GSH levels.
- FXN modulated apoptosis-related proteins (down-regulating Bax, up-regulating Bcl-2) and increased pAMPK levels, indicating activation of the AMPK pathway.
Conclusions:
- Fucoxanthin (FXN) demonstrates significant cardioprotective effects against high glucose-induced apoptosis by suppressing NADPH oxidase-mediated ROS production.
- FXN maintains the antioxidant defense system and protects cardiomyocytes from injury, partly through the activation of the AMPK cascade.
- The findings suggest FXN as a potential therapeutic agent for diabetic cardiomyopathy by targeting oxidative stress and apoptosis pathways.
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