Abstract
The aim of the present study was to assess the short-term effects of Thymoquinone (TQ) on oxidative stress, glycaemic control, and renal functions in diabetic rats. DM was induced in groups II and III with a single dose of streptozotocin (STZ), while group I received no medication (control). The rats in groups I and II were then given distilled water, while the rats in group III were given TQ at a dose of 50 mg/kg body weight/day for 4 weeks. Lipid peroxidase, nitric oxide (NO), total antioxidant capacity (TAC), glycated haemoglobin (HbA1c), lipid profiles, and renal function were assessed. Moreover, the renal tissues were used for histopathological examination. STZ increased the levels of HbA1c, lipid peroxidase, NO, and creatinine in STZ-induced diabetic rats in comparison to control rats. TAC was lower in STZ-induced diabetic rats than in the control group. Furthermore, rats treated with TQ exhibited significantly lower levels of HbA1c, lipid peroxidase, and NO than did untreated diabetic rats. TAC was higher in diabetic rats treated with TQ than in untreated diabetic rats. The histopathological results showed that treatment with TQ greatly attenuated the effect of STZ-induced diabetic nephropathy. TQ effectively adjusts glycaemic control and reduces oxidative stress in STZ-induced diabetic rats without significant damaging effects on the renal function.
Highlights
Diabetes mellitus (DM), a chronic metabolic disorder that is prevalent in humans, is associated with abnormally high levels of glucose in the blood
We demonstrated that inducing DM in Sprague-Dawley rats significantly disturbs the normal redox state, as was indicated by altered levels of lipid peroxidase, nitric oxide (NO), and total antioxidant capacity (TAC) in untreated diabetic rats relative to control rats
Sassy-Prigent et al [42], histopathology in the present study revealed that injecting rats with STZ resulted in glomerular hypertrophy, which could be largely attributed to mesangial expansion and the thickening of the glomerular basement membrane
Summary
Diabetes mellitus (DM), a chronic metabolic disorder that is prevalent in humans, is associated with abnormally high levels of glucose in the blood. Elevated glucose levels increase oxidative stress [1] by stimulating various mitochondrial enzymes, which results in the overproduction of reactive oxygen species (ROS) [2] and has detrimental effects on many organs [3]. Recent studies have shown that β-cell dysfunction in diabetic patients is mostly the result of enhanced oxidative stress [1,5]. When exploring the efficacy of anti-diabetic drugs, having antioxidant effects [8,9], efficacy in correcting dyslipidaemia [10] and hyperglycaemia [11], as well as safety, are crucial
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