Beneficial role of amygdalin extracts against animal growth regulator Boldjan induced cardiac toxicity, injury and oxidative stress in male rats

杏仁苷 氧化应激 丙二醛 肌酸激酶 内科学 内分泌学 毒性 胆固醇 高密度脂蛋白 乳酸脱氢酶 谷胱甘肽 药理学 医学 化学 生物化学 病理 替代医学
作者
Eman Mohammed Hussain,Sura Alkadhimy,Asmaa Maan Neamah,Ehab Tousson
出处
期刊:Toxicology Research [Oxford University Press]
卷期号:13 (2) 被引量:1
标识
DOI:10.1093/toxres/tfae042
摘要

Abstract Millions of individuals have used illicit anabolic-androgenic steroids (AAS), but the long-term cardiovascular associations of these drugs remain incompletely understood. Boldjan is AAS medication which is used in veterinary medicine and by young adults aiming to have a better appearance improving their self-esteem. Therefore; the objective of the current investigation was to examine any potential preventative effects of amygdalin extract against anabolic steroid Boldjan induced cardic toxicity, injury and oxidative stress in male rat. Forty adult male Wistar rats were classified into five groups (Gp1, Control Gp; Gp2, Amygdalin Gp in which rats treated with amygdalin (100 mg/kg body weight/day) daily for 2 weeks; Gp3, Boldjan Gp in which rats treated with Boldjan (10 mg/Kg BW/week) for 4 weeks; Gp4, Boldjan + Amygdalin). Boldjan induced a significant rises in serum lactate dehydrogenase (LDH), creatine kinase (CK) and creatine kinase MB (CK MB), aspartate aminotransferase (AST), total cholesterol (TC), triglycerides (TG), low-density lipoprotein-cholesterol (LDL-C), and very-low-density lipoprotein–cholesterol (VLDL-C), cardiac injury, and malondialdehyde (MDA) levels and a significant depletion in serum high-density lipoprotein-cholesterol (HDL-C), cardiac reduced glutathione (GSH), Superoxide dismutase (SOD) and catalase (Cat) activities as compared to control Gp. In contrast, Amygdalin significantly reversed the Boldjan induced cardiac toxicity in post treated rats Gp (Boldjan + Amygdalin). Amygdalin could be an efficient preventive supplement for mitigating Boldjan induced cardiac toxicity, possibly via controlling oxidative stress events.

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