article · Oxidative Medicine and Cellular Longevity
Diabetic cardiomyopathy is a severe complication linked to oxidative stress injuries. Oral administration of thymoquinone was evaluated in male diabetic rats over a twelve-week period. Thymoquinone treatment normalised critical plasma cardiac markers, specifically troponin I and creatine kinase, whilst restoring healthy lipid profiles by reducing triacylglycerol and low-density lipoprotein cholesterol and increasing high-density lipoprotein cholesterol. The compound improved cardiac antioxidant capacity, significantly elevating total superoxide dismutase activity and decreasing malondialdehyde levels. Furthermore, thymoquinone suppressed key inflammatory indicators, including C-reactive protein, interleukin-6, and E-selectin. Molecular analysis confirmed that thymoquinone downgraded cardiac-inducible nitric oxide synthase and upregulated vascular endothelial growth factor, erythropoietin genes, and nuclear factor-erythroid-2-related factor 2 protein, establishing that it protects cardiac muscles against diabetic damage through coordinated antioxidant and anti-inflammatory mechanisms.
Diabetic cardiomyopathy remains a major health challenge caused by chronic metabolic disturbances, oxidative stress, and inflammation. Demonstrating that a bioactive compound such as thymoquinone can reverse cardiac damage and reduce inflammation in living models provides valuable biological evidence. These findings highlight clear molecular pathways that could inform future interventions designed to preserve heart function in patients managing diabetes.
The findings suggest potential therapeutic applications for thymoquinone in drug discovery programmes focused on diabetic cardiovascular complications. Target users would primarily be biopharmaceutical developers and cardiovascular researchers seeking candidates that target oxidative stress pathways. However, because the evidence is restricted to an animal model involving twelve weeks of treatment in rats, the research remains at an early preclinical stage and is distant from clinical deployment.
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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 (<i>n</i> = 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.
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DOI: 10.1155/2018/7845681
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