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荜茇酮通过脂质调节信号通路对高胆固醇饮食诱导的动脉粥样硬化的保护作用。

Protective effects of zingerone on high cholesterol diet-induced atherosclerosis through lipid regulatory signaling pathway.

机构信息

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.

出版信息

Hum Exp Toxicol. 2021 Oct;40(10):1732-1745. doi: 10.1177/09603271211006170. Epub 2021 Apr 12.

Abstract

AIM

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.

METHODS

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.

RESULTS

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.

CONCLUSION

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.

摘要

目的

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。

方法

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。

结果

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。

结论

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。

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