The Falconoid Luteolin Mitigates the Myocardial Inflammatory Response Induced by High-Carbohydrate/High-Fat Diet in Wist
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ORIGINAL ARTICLE
The Falconoid Luteolin Mitigates the Myocardial Inflammatory Response Induced by High-Carbohydrate/High-Fat Diet in Wistar Rats Nashwa Abu-Elsaad1,3 and Amr El-Karef2
Luteolin is a major component of many medicinal plants and traditional medicines. The current study aims at testing its protective effect against high-carbohydrate/highfat (HCHF) diet-induced cardiac dysfunction in rats. Male Wistar rats were divided into six groups as follows: control group that received standard rat chow, group received HCHF diet (~ 30% carbohydrate and 42% fat) daily for 16 weeks, and four groups received HCHF diet concurrently with luteolin (10, 25, 50 or 100 mg/kg; 10% w/v suspension in 0.9% NaCl) daily from the first week by oral gavage. Body weight was measured weekly. At the end of the study, histopathological examinations of stained heart sections were carried out. Lipid profile, oxidative stress, and cardiac function biomarkers were measured. Furthermore, neurohumoral mediators and inflammatory cytokines (TNF-α, IL-18) were assigned. Results showed a significant improvement in cardiac function, tissue integrity, and a decrease in the compensatory neurohumoral mediators by luteolin 50 and 100 mg/kg. In addition, a significant (P < 0.05) decrease in collagen deposition, fibrosis percentage, lipid peroxidation, and inflammatory cells (macrophages and lymphocytes) infiltration was observed. Tested doses of luteolin decreased lipid peroxidation and elevated the endogenous antioxidant biomarkers (reduced glutathione and superoxide dismutase) significantly (P < 0.05). Finally, luteolin decreased TNF-α and IL-18 (P < 0.001) in a dose-dependent manner. It can be concluded that luteolin has a cardioprotective effect against HCHF diet-induced myocardial inflammation through antioxidant anti-inflammatory mechanisms. Abstract—
KEY WORDS: luteolin; cardiomyopathy; TNF-α; IL-18; high-fat diet.
INTRODUCTION Cardiovascular diseases remain the main cause of deaths worldwide. Metabolic syndrome and obesity are known to increase mortality and morbidity associating 1
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt 2 Department of Pathology, Faculty of Medicine, Mansoura University, Mansoura, 35516, Egypt 3 To whom correspondence should be addressed at Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt. E-mail: [email protected]
cardiovascular diseases [1–3]. Accordingly, modification in lipid metabolism in response to dietary lipid is a hallmark in keeping normal cardiac function [4]. In the last 20 years, many evidences have raised supporting the central role of the myocardial inflammatory response induced by high-carbohydrate high-fat diet in all phases of cardiomyopathy and atherosclerotic process [5, 6]. There is a direct correlation between the incidence of ischemic events and the increased release of some proinflammatory cytokines as tumor necrosis factor (TNF)-α and some interleukins (e.g., IL-18) [7, 8]. Giugl
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