Abstract
Diabetic cardiomyopathy is a diabetic complication due to oxidative stress injuries. This study examined the protecting influence of thymoquinone (TQ) on diabetes-caused cardiac complications. The intracellular means by which TQ works against diabetes-caused cardiac myopathy in rats is not completely understood. In this study, Wistar male rats (n = 60) were assigned into four groups: control, diabetic (diabetes induced by IP infusion of streptozotocin, 65 mg/kg), diabetic + TQ (diabetic rats given TQ (50 mg/kg) administered once per day by stomach gavage), and TQ (50 mg/kg) for 12 weeks. TQ supplementation appreciably recovered the cardiac parameters alongside significant declines in plasma nitric oxide concentrations and total superoxide dismutase (T.SOD) activities. Importantly, TQ downgraded expression of cardiac-inducible nitric oxide synthase in addition to significantly upregulating vascular endothelial growth factor and erythropoietin genes and nuclear factor-erythroid-2-related factor 2 (Nrf2) protein. TQ normalized plasma triacylglycerol and low-density lipoprotein-cholesterol and significantly improved the high-density lipoprotein-cholesterol levels. Additionally, TQ administration improved the antioxidant ability of cardiac tissue via significantly increased cardiac T.SOD and decreased cardiac malondialdehyde levels. Oral supplementation with TQ prevented diabetic-induced cardiomyopathy via its inhibitory effect on the E-selectin level, C-reactive protein, and interleukin-6. The TQ protecting effect on the heart tissue was shown by normalization of the plasma cardiac markers troponin I and creatine kinase. This experiment shows the aptitude of TQ to protect cardiac muscles against diabetic oxidative stress, mainly through upregulation of Nrf2, which defeated oxidative damage by improvement of the antioxidant power of cardiac muscle that consequently protected the cardiac muscles and alleviated the inflammatory process.
Highlights
Diabetes mellitus (DM) is a metabolic ailment that occurs due to different factors including either genetic or environmental influences
Plasma T.SOD activities were significantly reduced in the diabetic rats matched with control and TQ groups, which might be owing to damage due to diabetes (Figure 1(g))
Reduced when compared to control rats. These findings are consistent with results of Ighodaro et al [23] and Zhang et al [24] in which the authors reported significant elevations in total cholesterol, TAG, high-density lipoprotein-cholesterol (HDL-C), and Low-density lipoprotein-cholesterol (LDL-C) of STZ-treated rats, and with our previous results that the plasma concentration of insulin was significantly reduced in diabetic rats, which led to hyperglycemia with a high percentage of HbA1C [13]
Summary
Diabetes mellitus (DM) is a metabolic ailment that occurs due to different factors including either genetic or environmental influences. DM is distinguished by disturbances in insulin metabolism that alter carbohydrates, lipids, and protein metabolisms [1]. A cascade of myocardial variations that occur in DM with fibrosis, hypertrophy, and microcirculatory imperfections characterizes diabetic cardiomyopathy. These circulatory complaints hinder the heart efficiency, concomitantly result in cardiac failure [2]. Diabetic-induced cardiac complication is distinguished by myocardial functional alterations in which oxidative stresses are the main cause [3].
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