Li Fengyue, Lei Chunxia
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.
Arch Med Sci. 2020 Apr 15;21(1):272-284. doi: 10.5114/aoms.2020.94432. eCollection 2025.
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.
For the study, I 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.
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.
糖尿病性心肌病（DC）与舒张功能受损有关。高血糖介导的氧化应激和细胞凋亡是导致DC的主要因素。此外，NADPH氧化酶是心脏细胞或心肌细胞中活性氧（ROS）的主要来源。在此，我们评估了岩藻黄质（FXN）对高糖培养的新生大鼠心肌细胞的影响。
在本研究中，将新生大鼠心肌细胞在有或无FXN的情况下培养于高糖环境（30 mM/l）中。研究了细胞凋亡、细胞活力、NADPH氧化酶活性及其亚基的表达水平、丙二醛（MDA）水平和内源性抗氧化酶活性。我们还通过研究心肌细胞中AMPK、GSK-3β和Akt的表达来确定相关途径。
高糖环境增加了ROS的产生，而FXN通过抑制培养的新生大鼠心肌细胞中的ROS降低了氧化负担。FXN抑制了NADPH氧化酶的活性，Rac1也增加了其亚基的表达。FXN处理逆转了MDA、CAT、GSHpx、SOD活性和GSH含量。FXN下调了Bax水平，上调了Bcl-2（抗凋亡蛋白）水平；该处理保护心肌细胞免受损伤。此外，FXN增加了高糖处理的心脏细胞中pAMPK的水平。AMPK的药理学抑制剂消除了FXN在高糖诱导的心肌细胞中的活性。
FXN通过抑制NADPH氧化酶介导的ROS产生并维持组织中的抗氧化防御，对高糖介导的心脏细胞凋亡发挥保护作用。FXN的衰减活性通过AMPK级联传导。
