Myosins Are Differentially Expressed under Oxidative Stress in Chronic Streptozotocin-Induced Diabetic Rat Brains.
Luciana Karen CalábriaAlice Vieira da CostaRenato José da Silva OliveiraSimone Ramos DeconteRafael NascimentoWashington João de CarvalhoVanessa Neves de OliveiraCarlos Alberto ArcaroLuciana Rezende Alves de OliveiraLuiz Ricardo GoulartFoued Salmen EspindolaPublished in: ISRN neuroscience (2013)
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.
Keyphrases
- diabetic rats
- oxidative stress
- ischemia reperfusion injury
- dna damage
- induced apoptosis
- type diabetes
- binding protein
- cardiovascular disease
- signaling pathway
- poor prognosis
- glycemic control
- cell proliferation
- gene expression
- transcription factor
- hydrogen peroxide
- brain injury
- subarachnoid hemorrhage
- nitric oxide
- cerebral ischemia
- anti inflammatory
- endothelial cells
- pi k akt
- insulin resistance
- high fat diet
- blood brain barrier
- small molecule
- functional connectivity
- weight loss
- protein protein