Effect of Microencapsulated and Nonencapsulated Aronia Extract on Paraoxonase 1 Gene Expression and Aortic Histopathology in High-Fat Diet-Fed Rats

The aim of this study was to determine the effects of microencapsulated and nonencapsulated aronia (<i>Aronia melanocarpa</i>) extract on paraoxonase 1 (PON1) mRNA expression, HDL cholesterol, and aortic atherosclerosis in rat blood and liver tissues. The study involved 42 male Sprague-Dawley rats aged 10 weeks. The experimental groups were as follows: (1) standard diet control (CON), (2) high-fat diet (HF) control, (3) HF + 400 mg/kg aronia extract (HF400E), (4) HF + 200 mg/kg aronia extract (HF200E), (5) HF + 400 mg/kg microencapsulated aronia (HF400C), and (6) HF + 200 mg/kg microencapsulated aronia (HF200C). The rats were fed a HF between the 10th and 20th week, and at the end of the 20th week, all groups except CON were administered aronia extract (200-400 mg/kg) by oral gavage for 6 weeks. After 6 weeks, biochemical analyses and aortic histology evaluations were performed. The results showed that the HF significantly increased serum total cholesterol, triglycerides, low-density lipoprotein levels, and hepatic malondialdehyde levels. However, administration of HF400E significantly reduced these parameters in hyperlipidemic rats. Serum PON1 enzyme activity was significantly higher in the HF400E group compared with both the CON (<i>P</i> < .001) and HF (<i>P</i> < .0025) groups. Although PON1 mRNA levels in the HF400E, HF200E, and HF200C groups were higher than in the CON and HF groups, the differences were not statistically significant. Evaluation of the aortic tissues showed normal tissue morphology in all experimental groups, with no signs of atherosclerotic plaques, hyaline or mucoid changes, or endothelial anomalies in the thoracic or aortic arch tissues. These findings suggest that aronia, rich in anthocyanins and other polyphenolic compounds, may help prevent and slow down atherosclerosis by enhancing PON1 enzyme activity, which is involved in preventing lipid oxidation, the first step in atherosclerosis.