Diabetes mellitus (DM) constitutes one of the public health problems today. It is characterized by hyperglycemia through a defect in the β-cells function and/or decreased insulin sensitivity. Apocynin has been tasted acting directly as an NADPH oxidase inhibitor and reactive oxygen species (ROS) scavenger, exhibiting beneficial effects against diabetic complications. Hence, the present study’s goal was to dissect the possible mechanisms by which apocynin could mediate its cardioprotective effect against DM-induced oxidative stress. Male Wistar rats were assigned into 4 groups: Control (C), control + apocynin (C+A), diabetes (D), diabetes + apocynin (D+A). DM was induced with streptozotocin. Apocynin treatment (3 mg/kg/day) was applied for 5 weeks. Treatment significantly decreased blood glucose levels and insulin resistance in diabetic rats. In cardiac tissue, ROS levels were higher, and catalase enzyme activity was reduced in the D group compared to the C group; the apocynin treatment significantly attenuated these responses. In heart mitochondria, Complexes I and II of the electron transport chain (ETC) were significantly enhanced in the D+A group. Total glutathione, the level of reduced glutathione (GSH) and the GSH/ oxidized glutathione (GSSG) ratio were increased in the D+A group. Superoxide dismutase (SOD) and the glutathione peroxidase (GSH-Px) activities were without change. Apocynin enhances glucose uptake and insulin sensitivity, preserving the antioxidant defense and mitochondrial function.
Chronic hyperglycemic state during diabetes mellitus (DM) has been related to an increase in oxidative stress, which causes damage to skeletal muscle tissue, contributing to the appearance of muscle fatigue, characterized by decreased strength. An increase in the activity of the enzyme NADPH oxidase 2 (NOX2) has been observed in skeletal muscle, and with it an increase in basal ROS production; It has been linked to the alteration of insulin signaling in tissue. Consequently, normal muscle metabolism is affected, compromising the ability of individuals to perform physical activity. Apocynin is a drug that, in addition to being a specific inhibitor of NADPH oxidase, has antioxidant properties reported in experimental models of insulin resistance. However, the effect of NOX2 inhibition on skeletal muscle health during DM is unknown. Therefore, in order to preserve muscle structure and function, the objective of this study was to evaluate the effect of NOX2 inhibition by apocynin on muscle function in an experimental diabetes model. Male Wistar rats (230–250 g) were randomly divided into four groups, among them: control, apocynin control, diabetic and apocynin diabetic, in which diabetes was induced intraperitoneally with streptozotocin (45 mg / kg). Treatment with apocynin (3 mg / kg / day) was administered for 8 weeks and at the end of the treatment, the extensor digitorum longus (EDL) muscles were isolated and an isometric tension protocol was performed (repetitive electrical stimulation: pulses of 100 V, 300 ms duration and frequency 45 and 50 Hz, respectively). Treatment with apocynin contributed to a significant increase in the time of resistance to fatigue (88.23%; p <0.05) and improved the maximum muscle tension (72.23%; p <0.5) and total (80%; p <0.5) compared to the diabetic group. Additionally, a positive effect on weight and a decrease in blood glucose level was observed. Together, these results indicate that NOX2 inhibition exerted a protective effect on skeletal muscle tissue during diabetes.
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