Olive oil protects against cardiac hypertrophy in D-galactose induced aging rats.

BACKGROUND

Aged heart is defined via structural and mitochondrial dysfunction of the heart. However, there is still no potent compound to improve cardiac function abnormalities in aged individuals. Olive oil (OLO), as an oil with monounsaturated fatty acids, has diverse protective effects on the cardiovascular system, including anti-inflammatory, anti-diabetic, and mitigating effects on blood pressure. In the present study, we evaluated the protective effects of OLO against aging-related cardiac dysfunction.

METHODS

Male Wistar rats were randomly divided into three groups: Control, D-galactose-induced aging rats (D-GAL group), and aging rats treated with OLO (D-GAL + OLO group). Aging in rats was induced by intraperitoneal injection of D-GAL at 150 mg/kg dose for eight weeks and the D-GAL + OLO group was treated with oral OLO by gavage for eight weeks. The heart tissues were harvested to assay the oxidative stress, molecular parameters, and histological analysis.

RESULTS

The D-GAL given rats indicated increased cardiomyocyte diameter as cardiac hypertrophy marker (21 ± 0.8, p < 0.001), an increased Malondialdehyde (MDA) level (27 ± 3, p < 0.001), a reduced Superoxide dismutase (SOD) (p < 0.001, 18.12 ± 1.3), and reduction in gene expression of Sirtuin 1 (SIRT1) (p < 0.05, 0.37 ± 0.06), Peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1α (p < 0.001, 0.027 ± 0.04), and Transcription Factor A, Mitochondrial (TFAM) (p < 0.001, 0.023 ± 0.01), Bcl2 (p < 0.001, 0.04 ± 0.004) and an increase in gene expression of Bax (p < 0.001, 23.5 ± 5.4) in comparison with the control animals. Treatment with OLO improved cardiac hypertrophy (14 ± 0.4, p < 0.001), MDA (22 ± 2.5, p < 0.01), SOD (p < 0.001, 34.9 ± 2), SIRT1 (p < 0.05, 1.37 ± 0.46), PGC-1α (p < 0.001, 1.11 ± 0.1), TFAM (p < 0.01, 0.23 ± 0.02), Bcl2 (p < 0.05, 0.35 ± 0.05) and Bax genes (p < 0.01, 0.1 ± 0.03).

CONCLUSIONS

Overall, OLO protects the heart against D-GAL-induced aging via increasing antioxidant effects, and enhancing cardiac expression of SIRT1, PGC-1α, TFAM, Bcl2 and Bax genes.