Thymoquinone Attenuates Cardiomyopathy in Streptozotocin‐Treated Diabetic Rats

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.

Protective Effect of Hydroxysafflor Yellow A on Nephropathy by Attenuating Oxidative Stress and Inhibiting Apoptosis in Induced Type 2 Diabetes in Rat

“…Furthermore, reduction in hypertriglyceridemia applying fibrates therapy can abate UAER rise in T2DM patients [37]. Expectingly, HSYA can significantly lower the level of blood lipid profile in T2DM rats in our study, which has a similar result with the previous study [38]. Taken together, HSYA could ameliorate hyperlipemia and suppresses the inflammatory response by reducing the accumulation of inflammatory product.…”

<p>Effects of Hydroxysafflor Yellow A on the PI3K/AKT Pathway and Apoptosis of Pancreatic β-Cells in Type 2 Diabetes Mellitus Rats</p>

“…Feeding with HFD could induce hyperlipemia and insulin resistance, 20,21 HSYA-treatment not only decreased FBG but had the anti-hyperlipidemic effect which would improve insulin resistance indirectly. Although HDL-C had the antioxidant and anti-inflammatory effects 22 and some studies 23,24 showed that the HDL-C level in T2DM rats would be higher than that of the normal rats, our founding suggested that there was no statistical difference between them as the previous study. 25 In this study, the T2DM rats indicated a decrease in acinar staining intensity that reflecting the defects in digestive function of the pancreas.…”

Thymoquinone protects against hyperlipemia-induced cardiac damage in low-density lipoprotein receptor-deficient (LDL-R−/−) mice

“…In addition, TQ alleviates diabetes-associated oxidative stress in cardiac tissues [8]. Additionally, several studies have shown that the protective effect of TQ against cardiac damage such as in case of ischemic damage [9] and acute abdominal aortic ischemia-reperfusion injury [10]is mediated via the pyroptosis pathway [11].…”