Abstract

Context: Polyphenols and flavonoids in artichoke leaf tincture (ALT) protect cells against oxidative damage.Objectives: We examined ALT effects on deoxyribonucleic acid (DNA) damage and lipid profiles in rat plasma and gene expression in rat aorta [haemeoxygenase-1 (HO1), haemeoxygenase-2 (HO2), NADPH oxidase 4 (NOX-4), monocyte chemoattractant protein-1 (MCP-1) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2)].Materials and methods: Eighteen male Wistar albino rats were divided into three groups (n = 6/group): The control group (CG) was fed with standard pellet chow for 11 weeks; the AD group was fed for a similar period of time with pellet chow supplemented with 2% cholesterol, 3% sunflower oil and 1% sodium cholate. The ADA group was fed with pellet chow (for 1 week), the atherogenic diet (see above) for the following 4 weeks and then with ALT (0.1 mL/kg body weight) and atherogenic diet for 6 weeks. According to HPLC analysis, the isolated main compounds in ALT were chlorogenic acid, caffeic acid, isoquercitrin and rutin.Results: Normalized HO-1 [0.11 (0.04–0.24)] and MCP-1 [0.29 (0.21–0.47)] mRNA levels and DNA scores [12.50 (4.50–36.50)] were significantly lower in the ADA group than in the AD group [0.84 (0.35–2.51)], p = 0.021 for HO-1 [0.85 (0.61–3.45)], p = 0.047 for MCP-1 and [176.5 (66.50–221.25)], p = 0.020 for DNA scores. HO-1 mRNA was lower in the ADA group than in the CG group [0.30 (0.21–0.71), p = 0.049].Conclusions: Supplementation with ALT limited the effects of the atherogenic diet through reduced MCP-1 expression, thereby preventing oxidative damage.

Highlights

  • Current data inform us that the most common causes of death worldwide are atherosclerosis-associated diseases (Hansson 2005; Go et al 2014), evidence suggests that common risk factors for atherosclerosis, such as hypercholesterolemia (Jandaghi et al 2016; Yousefi et al 2017), hypertension (Ardalani et al 2016), obesity (Furukawa et al 2017; Niemann et al 2017), a sedentary way of life (Gomez-Cabrera et al 2008) and smoking (Niemann et al 2017), all increase the production of free reactive oxygen species (ROS) which leads to oxidative modification of deoxyribonucleic acid (DNA), proteins and lipids, causing changes in their regular functions (De Bont and Van Larebeke 2004) which can contribute to further escalation of atherosclerotic processes (Harman 1956)

  • To further understand the effect of a lipid-rich diet and a lipid-rich diet containing artichoke leaf tincture (ALT) on pathways that contribute to atherosclerotic processes, we investigated the expression of several genes [transcription factor nuclear factor (erythroidderived 2)-like 2 (Nrf2), cytoprotective enzymes (HO-1, HO-2), nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX-4) and monocyte chemoattractant protein-1 (MCP-1)] in rat aorta

  • Gene expression of HO1, HO2, NOX-4, MCP-1 and Nrf2 were measured in rat aortas

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Summary

Introduction

Current data inform us that the most common causes of death worldwide are atherosclerosis-associated diseases (Hansson 2005; Go et al 2014), evidence suggests that common risk factors for atherosclerosis, such as hypercholesterolemia (Jandaghi et al 2016; Yousefi et al 2017), hypertension (Ardalani et al 2016), obesity (Furukawa et al 2017; Niemann et al 2017), a sedentary way of life (Gomez-Cabrera et al 2008) and smoking (Niemann et al 2017), all increase the production of free reactive oxygen species (ROS) which leads to oxidative modification of deoxyribonucleic acid (DNA), proteins and lipids, causing changes in their regular functions (De Bont and Van Larebeke 2004) which can contribute to further escalation of atherosclerotic processes (Harman 1956). Several phytochemicals present in the artichoke leaf regulate the expression of genes involved in cellular defence by the activation of nuclear factor (erythroidderived 2)-like 2 (Nrf2) (Jeong et al 2006). The majority of data regarding the role of polyphenols and flavonoids in artichoke leaf on gene expression in atherosclerosis are from in vitro studies. The number of studies in animal models is limited

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