BMC cardiovascular disorders · 2024
Olive oil protects against cardiac hypertrophy in D-galactose induced aging rats.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Shahidi Siamak, Ramezani-Aliakbari Khadijeh, Sarihi Abdolrahman, Heshmati Ali, Shiri Elham, Nosrati Shiva, Hashemi Sayedpayam, Bahrami Mitra, Ramezani-Aliakbari Fatemeh
Аннотация
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.
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.
Предметные рубрики MeSH
AnimalsMaleGalactoseRats, WistarOxidative StressOlive OilAgingDisease Models, AnimalSirtuin 1Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAntioxidantsAge FactorsApoptosisMyocytes, CardiacTranscription FactorsApoptosis Regulatory ProteinsProto-Oncogene Proteins c-bcl-2Ventricular Remodeling