Abstract
Context: Lutein (LU) is a major carotenoid with various pharmacological activities including anti-inflammatory, antioxidant and anti-apoptosis.Objective: The cardioprotective efficacy of LU was determined by evaluating the biochemical and histopathological changes in isoproterenol (ISO) induced myocardial infarction (MI) rat model.Materials and methods: Healthy male albino rats (n = 40) were segregated into 4 equal groups. Group I (control) rats were administered with olive oil, Group II (LU) rats were orally pre-treated with only 40 mg of LU for 28 days, Group III (MI induced) rats were injected (subcutaneously; s.c) with 85 mg/kg of ISO for 2 consecutive days, whereas Group IV (LU + ISO) rats were pre-treated with 40 mg of LU for 28 days before ISO induction.Results: ISO-induced group showed increased infarct size and cardiac/inflammatory/apoptotic markers. However, pre-treatment with LU (28 days) considerably reduced (p < 0.01) the infarct size (14%), lipid peroxidation product (MDA;42%), cardiac markers [(lactate dehydrogenase (LDH) and creatine kinase-MB (CK-MB), cardiac troponin T (cTn T)], inflammatory markers [IL-1β, IL-6, tumour necrosis factor alpha (TNF-α), nuclear factor kappa B p65 subunit (NF-κB p65)] and apoptotic markers (caspase-3 and -9). Also, LU significantly improved (p < 0.01) the antioxidants [catalase (CAT), superoxide dismutase (SOD)] as well as markedly upregulated (p < 0.01) the protein expression of HO-1 and Nrf2. Moreover, LU considerably reversed all the histopathological changes and thus exhibits its cardioprotective activity.Conclusion: LU exhibits potent cardioprotective activity against ISO-induced cardiotoxicity and might be recommended with standard cardioprotective agents for treating various MI-related complications.
Highlights
Heart attack or myocardial infarction (MI) is one of the deadliest forms of ischaemic heart disease as it results in high mortality and morbidity
China Heart Failure Symposium/ Association and World Health Organization (WHO) reported that approximately 50% of total cardiovascular disease (CVD)related mortality is due to MI (Li et al 2015a)
MI is caused by insufficient oxygenated blood flow to the myocardium which results in an imbalance in oxygen/nutrient demand and eventually leads myocardial damage or injury (Amran et al 2015)
Summary
Heart attack or myocardial infarction (MI) is one of the deadliest forms of ischaemic heart disease as it results in high mortality and morbidity. MI is caused by insufficient oxygenated blood flow to the myocardium (via a coronary artery) which results in an imbalance in oxygen/nutrient demand and eventually leads myocardial damage or injury (Amran et al 2015). Many scientists have demonstrated various pathophysiological and biochemical events including oxidative stress (lipid peroxidation), inflammatory response, necrosis, apoptosis, hyperlipidaemia, etc. The current treatment regimen for MI (anti-thrombotic/anti-coagulant) is very limited as it triggers various serious adverse effects including heartburn, hypertension, gastrointestinal disorders. There is a quest for novel natural cardio-therapeutic agents with potent antioxidant, anti-inflammatory and antiapoptotic properties that would limit or protect myocardial injury or damage with no or fewer adverse effects (Upaganlawar et al 2011; Wong et al 2017)
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