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ORIGINAL ARTICLE
Year : 2021  |  Volume : 12  |  Issue : 1  |  Page : 45

Preventive effect of eucalyptol on the formation of aorta lesions in the diabetic-atherosclerotic rat


1 Department of Clinical Biochemistry, Faculty of Medicine, Ardabil University of Medical Sciences, Ardabil, Iran
2 Department of Endocrinology and Metabolism, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Correspondence Address:
Sina Mahdavifard
Department of Clinical Biochemistry, Faculty of Medicine, Ardabil University of Medical Sciences, Ardabil
Iran
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijpvm.IJPVM_319_19

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Background: Glycation, inflammation, and oxidative stress are the cardinal motivators of diabetes vascular complications. Here, we studied the effect of eucalyptol (EUC) on the formation of atheromatous lesions, glycation, oxidative stress, and inflammatory markers as well as insulin resistance, lipid profile, and activity of glyoxalase-1 (GLO-I) in the atherosclerotic rat model. Methods: Diabetic-atherosclerosis induced in rats with a combination of streptozotocin and atherogenic diet. Two groups of rats, normal and diabetic-atherosclerotic, were treated intragastrically with EUC (200 mg/kg) once daily for 3 months. Fasting blood sugar (FBS), insulin, insulin resistance index, lipid profile, the activity of GLO-I, low-density lipoprotein (LDL) glycation and oxidation markers, inflammatory markers, creatinine in the serum, and proteinuria in the urine of all rats were determined. Results: EUC inhibited the formation of any atheromatous lesions in atherosclerotic rats. Further, EUC displayed the lowering effect on glycemia, insulin resistance, LDL glycation, and oxidation products, and tumor necrosis factor (TNF)-α as well as it exhibited the improving effect on lipid profile, the activity of GLO-I, and renal function in the diabetic rat (P < 0.001). Conclusions: EUC prevented the formation of the atheromatous lesions and improved renal function in the atherosclerotic rat model due to a reduction of glycation, oxidative stress, and inflammatory mediators.


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