Dong Min, Luo Yao, Lan Yong, He Qinghua, Xu Lei, Pei Zuowei
Department of Cardiology, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, 100730, China.
Department of Vascular Surger, Beijing Hospital, National Center of Gerontology, Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing, 100730, China.
Heliyon. 2023 Jun 23;9(6):e17613. doi: 10.1016/j.heliyon.2023.e17613. eCollection 2023 Jun.
Hyperlipidemia is a risk factor for cardiac damage that can lead to many cardiovascular diseases. A recent study reported the cardioprotective effects of luteolin and . In this study, we aimed to investigate the possible protective effects of luteolin against hyperlipidemia-induced cardiac damage in Sprague-Dawley (SD) rats.
Six-week-old male SD rats were randomly divided into five groups: a normal diet (ND) group; a high-fat diet (HFD) group; and three high-fat diet mixed with luteolin (HFD + LUT) groups, where in a luteolin dosage 50, 100, or 200 mg/kg/day was administered. All groups were fed their respective diets for 12 weeks.
Left ventricular ejection fraction and fractional shortening (parameters of cardiac function) were lower in the HFD + LUT (100 mg/kg/day) group than in the HFD group. Metabolic parameters were lower in the HFD + LUT (100 mg/kg/day) group than in the HFD group. Collagen I, collagen III, and TGF-β expression levels were lower in the cardiac tissues of the HFD + LUT (100 mg/kg/day) group, compared to those of the HFD group. Expression of the profibrotic genes MMP2 and MMP9 was suppressed in the cardiac tissues of the HFD + LUT (100 mg/kg/day) group, compared to those of the HFD group. Furthermore, CD36 and lectin-like oxidized low-density lipoprotein receptor-1 protein levels were lower in the cardiac tissues of the HFD + LUT (100 mg/kg/day) group, compared to those of the HFD group.
These findings would provide new insights into the role of luteolin in hyperlipidemia-induced cardiac damage and contribute to the development of novel therapeutic interventions to treat cardiovascular disease progression.
高脂血症是导致心脏损伤的危险因素,可引发多种心血管疾病。最近一项研究报道了木犀草素的心脏保护作用。在本研究中,我们旨在探讨木犀草素对高脂血症诱导的Sprague-Dawley(SD)大鼠心脏损伤的潜在保护作用。
将六周龄雄性SD大鼠随机分为五组:正常饮食(ND)组;高脂饮食(HFD)组;以及三个高脂饮食加木犀草素(HFD + LUT)组,分别给予50、100或200 mg/kg/天的木犀草素剂量。所有组均喂食各自的饮食12周。
HFD + LUT(100 mg/kg/天)组的左心室射血分数和缩短分数(心脏功能参数)低于HFD组。HFD + LUT(100 mg/kg/天)组的代谢参数低于HFD组。与HFD组相比,HFD + LUT(100 mg/kg/天)组心脏组织中的I型胶原、III型胶原和TGF-β表达水平较低。与HFD组相比,HFD + LUT(100 mg/kg/天)组心脏组织中促纤维化基因MMP2和MMP9的表达受到抑制。此外,与HFD组相比,HFD + LUT(100 mg/kg/天)组心脏组织中的CD36和凝集素样氧化低密度脂蛋白受体-1蛋白水平较低。
这些发现将为木犀草素在高脂血症诱导的心脏损伤中的作用提供新的见解,并有助于开发新的治疗干预措施以治疗心血管疾病进展。