Department of Emergency, 159363Tangshan Gongren Hospital, Tangshan, Hebei, People's Republic of China.
Medical Imaging Department, 159363Tangshan Gongren Hospital, Tangshan, Hebei, People's Republic of China.
Hum Exp Toxicol. 2021 Oct;40(10):1732-1745. doi: 10.1177/09603271211006170. Epub 2021 Apr 12.
A high cholesterol diet (HCD) is known to cause metabolic dysregulation, oxidative stress, cardiovascular diseases and atherogenesis. Zingerone is a pharmacologically active component of dry ginger. Zingerone has been shown to have a wide range of pharmacological properties, including scavenging free radicals, high antioxidant activity, suppressing lipid peroxidation and anti-inflammatory. This study aimed to investigate the effects of Zingerone on HCD-induced atherosclerosis in rats.
Animals were divided into four categories (n = 6). Group I: normal control, Group II: zingerone control (20 mg/kg b.wt.), group III: HCD-induced atherosclerosis, Group IV: HCD + zingerone, respectively, for 8 weeks.
The HCD-fed rats resulted in a significant increase in an atherosclerotic lesion, lipid peroxidation, lipid profile, high-density lipoprotein concentration, cardiac markers, body weight, reduced antioxidant status, and displayed atherosclerosis. These findings were conventional by up-regulated expression of lipid regulatory genes like sterol-regulatory-element-binding protein-c (SREBP-c), fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), acetyl-CoA synthetase (ACS), liver X receptor-alpha (LXR-α), and down-regulated expression of acetyl-CoA oxidase (ACO), peroxisome proliferator-activated receptor-alpha (PPAR-α) and carnitine palmitoyl transferase-1 (CPT-1) in HCD-fed rats. These significant changes were observed in the zingerone-treated rats for the last 4 weeks.
These findings suggest that zingerone reduced atherosclerosis by modulated the atherosclerotic lesion, lipid profile, antioxidant status and lipid regulatory gene expression in HCD-fed rats.
高胆固醇饮食(HCD)已知会导致代谢失调、氧化应激、心血管疾病和动脉粥样硬化形成。姜酮是干姜的一种具有药理活性的成分。姜酮具有广泛的药理特性,包括清除自由基、高抗氧化活性、抑制脂质过氧化和抗炎作用。本研究旨在探讨姜酮对 HCD 诱导的大鼠动脉粥样硬化的影响。
动物分为四组(n = 6)。第 I 组:正常对照组;第 II 组:姜酮对照组(20mg/kg 体重);第 III 组:HCD 诱导的动脉粥样硬化组;第 IV 组:HCD+姜酮组,分别喂养 8 周。
HCD 喂养的大鼠导致动脉粥样硬化病变、脂质过氧化、血脂谱、高密度脂蛋白浓度、心脏标志物、体重显著增加,抗氧化状态降低,并表现出动脉粥样硬化。这些发现被上调的脂质调节基因的表达所证实,如固醇调节元件结合蛋白-c(SREBP-c)、脂肪酸合酶(FAS)、乙酰辅酶 A 羧化酶(ACC)、乙酰辅酶 A 合成酶(ACS)、肝 X 受体-α(LXR-α),以及下调的乙酰辅酶 A 氧化酶(ACO)、过氧化物酶体增殖物激活受体-α(PPAR-α)和肉碱棕榈酰转移酶-1(CPT-1)在 HCD 喂养的大鼠中的表达。这些显著变化在最后 4 周用姜酮处理的大鼠中观察到。
这些发现表明,姜酮通过调节 HCD 喂养大鼠的动脉粥样硬化病变、血脂谱、抗氧化状态和脂质调节基因表达来减少动脉粥样硬化。