Myosins Are Differentially Expressed under Oxidative Stress in Chronic Streptozotocin-Induced Diabetic Rat Brains

Abstract

Diabetes mellitus is a disease characterized by persistent hyperglycemia, which may lead to brain tissue damage due to oxidative stress and also contributes to neuronal death and changes in synaptic transmission. This study evaluated the effect of oxidative stress and the use of antioxidants supplementation on myosins expression levels in the brains of chronic diabetic rats induced by streptozotocin. Lipid peroxidation, antioxidant enzymes activities, and myosins-IIB and -Va expressions at transcriptional and translational levels were examined after 90 days induction. The chronic effect of the diabetes led to the upregulation of superoxide dismutase (SOD) and catalase (CAT) activities, and the downregulation of glutathione peroxidase (GPx), but there was no statistically significant increase in the malondialdehyde (MDA) levels. These alterations were accompanied by high myosin-IIB and low myosin-Va expressions. Although the antioxidant supplementation did not interfere on MDA levels, the oxidative stress caused by chronic hyperglycemia was reduced by increasing SOD and restoring CAT and GPx activities. Interestingly, after supplementation, diabetic rats recovered only myosin-Va protein levels, without interfering on myosins mRNA levels expressed in diabetic rat brains. Our results suggest that antioxidant supplementation reduces oxidative stress and also regulates the myosins protein expression, which should be beneficial to individuals with diabetes/chronic hyperglycemia.

Lipid peroxidation and neuroinflammation: A possible link between maternal fructose intake and delay of acquisition of neonatal reflexes in Wistar female rats

“…In our study, CAT and SOD antioxidant defenses in the brain of the female offspring were enhanced at PN1. In agreement with these results, these antioxidant defenses were found to be elevated in the brain of diabetic induced models, in response to oxidative stress (Calábria et al, 2013;Huang et al, 1999), as well as in other organs during the early stages of diabetes (Dias et al, 2010;Kakkar et al, 1997). It is important to note that since oxidative stress typically varies over time, a longitudinal analysis is required to analyze the changes in both, the oxidative damage and antioxidant response in the offspring.…”

“…Our result suggests that the activations of SOD expression and CAT activity are an early putative protection mechanism of fructose‐induced oxidative stress. Fructose feeding has been reported to induce oxidative damage to lipids (Calábria et al., 2013; Cigliano et al., 2018). Our study shows enhanced lipid peroxidation (TBARS) in total brain of the female offspring.…”

Phytochemical characterization of the Vochysia rufa (Vochysiaceae) extract and its effects on oxidative stress in the pancreata of streptozotocin-induced diabetic rats

“…Animals were fasted for another 90 min after the injection. Ten days after the STZ injection, rats with a fasting blood glucose level greater than 250 mg/dL were used for subsequent experiments [ 16 , 17 ]. Body weight and blood glucose levels were monitored in animals undergoing the different treatments (water, glibenclamide, and V .…”

The Potential Role of Cytokines and Growth Factors in the Pathogenesis of Alzheimer’s Disease

“…Where the absence of superoxide dismutase (SOD) was observed to increase oxidation damage from ROS; an escalation of Ser-36 phospho-TAU was revealed in treatments of SOD null mice; untreated mice did not survive past one week, SOD deficiency was therefore deleterious [103]. Notably, an increase in myosin IIB (MIIB) was also found to mirror the increasing depletion of SOD activity in chronically diabetic rats [104].…”