College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, P.R. China.
College of Veterinary Medicine, Northeast Agricultural University, Harbin, 150030, P.R. China; Key Laboratory of the Provincial Education Department of Heilongjiang for Common Animal Disease Prevention and Treatment, Northeast Agricultural University, Harbin, P.R. China; Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, Northeast Agricultural University, Harbin 150030, P.R. China.
J Nutr Biochem. 2023 May;115:109285. doi: 10.1016/j.jnutbio.2023.109285. Epub 2023 Feb 14.
Di-(2-ethylhexyl) phthalate (DEHP) is a plasticizer that is easily found in the environment. Excessive daily exposure of it may lead to an increased risk of cardiovascular disease (CVD). Lycopene (LYC), as a natural carotenoid, has been shown to have the potential to prevent CVD. However, the mechanism of LYC on cardiotoxicity caused by DEHP exposure is unknown. The research was aimed to investigate the chemoprotection of LYC on the cardiotoxicity caused by DEHP exposure. Mice were treated with DEHP (500 mg/kg or 1,000 mg/kg) and/or LYC (5 mg/kg) for 28 d by intragastric administration, and the heart was subjected to histopathology and biochemistry analysis. The results indicated that DEHP caused cardiac histological alterations and enhanced the activity of cardiac injury indicators, and interfered with mitochondrial function and activating mitophagy. Notably, LYC supplementation could inhibit DEHP-induced oxidative stress. The mitochondrial dysfunction and emotional disorder caused by DEHP exposure were significantly improved through the protective effect of LYC. We concluded that LYC enhances mitochondrial function by regulating mitochondrial biogenesis and dynamics to antagonize DEHP-induced cardiac mitophagy and oxidative stress.
邻苯二甲酸二（2-乙基己基）酯（DEHP）是一种很容易在环境中找到的增塑剂。过量的日常暴露可能会增加心血管疾病（CVD）的风险。番茄红素（LYC）作为一种天然类胡萝卜素，已被证明具有预防 CVD 的潜力。然而，LYC 对 DEHP 暴露引起的心脏毒性的作用机制尚不清楚。本研究旨在探讨 LYC 对 DEHP 暴露引起的心脏毒性的化学保护作用。通过灌胃给予小鼠 DEHP（500mg/kg 或 1000mg/kg）和/或 LYC（5mg/kg）28d，对心脏进行组织病理学和生物化学分析。结果表明，DEHP 导致心脏组织学改变，增强了心脏损伤标志物的活性，并干扰了线粒体功能和激活自噬。值得注意的是，LYC 补充可以抑制 DEHP 诱导的氧化应激。通过 LYC 的保护作用，显著改善了 DEHP 暴露引起的线粒体功能障碍和情绪障碍。我们得出结论，LYC 通过调节线粒体生物发生和动力学增强线粒体功能，拮抗 DEHP 诱导的心脏自噬和氧化应激。
