Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2013 Sep 24:2013:423931.
doi: 10.1155/2013/423931. eCollection 2013.

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

Luciana Karen Calábria  1 , Alice Vieira da Costa  2 , Renato José da Silva Oliveira  2 , Simone Ramos Deconte  2 , Rafael Nascimento  2 , Washington João de Carvalho  2 , Vanessa Neves de Oliveira  3 , Carlos Alberto Arcaro Filho  4 , Luciana Rezende Alves de Oliveira  4 , Luiz Ricardo Goulart  2 , Foued Salmen Espindola  2
Affiliations

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

Luciana Karen Calábria et al. ISRN Neurosci. .

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.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Supplementation effects on antioxidant enzymes activity and lipid peroxidation in diabetic rat brain. Data are mean ± SEM, n = 4 rats/subgroup. Significant differences: *compared to nondiabetic (ND) (GPx and SOD- P < 0.001; CAT- P < 0.05); **diabetic (D) versus supplemented diabetic (SD) (GPx- P < 0.001; CAT- P < 0.05).
Figure 2
Figure 2
Supplementation and diabetes effects on myosin-IIB and myosin-Va protein levels in rat brains. The amount of myosin proteins showed on the immunoblot was determined densitometrically and expressed as a related percentage of the groups (n = 4 rats/subgroup). Values represent mean ± SEM. Significant differences: *compared to nondiabetic (ND) (Myosin-IIB- P < 0.05; Myosin-Va- P < 0.005); **diabetic (D) versus supplemented diabetic (SD) (Myosin-Va- P < 0.005).
Figure 3
Figure 3
Diabetes and supplementation effects on MYH10 and MYO5A mRNAs expression in rat brains. Relative expression of MYH10 and MYO5A mRNAs in brain samples of diabetic (D) and supplemented diabetic (SD) compared to nondiabetic (ND) rats. (*) P < 0.05. Values represent mean ± SEM (n = 4 rats/subgroup).
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

References

    1. Lamb RE, Goldstein BJ. Modulating an oxidative-inflammatory cascade: potential new treatment strategy for improving glucose metabolism, insulin resistance, and vascular function. International Journal of Clinical Practice. 2008;62(7):1087–1095. - PMC - PubMed
    1. Nishikawa T, Edelstein D, Du XL, et al. Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage. Nature. 2000;404(6779):787–790. - PubMed
    1. Brands AMA, Kessels RPC, de Haan EHF, Kappelle LJ, Biessels GJ. Cerebral dysfunction in type 1 diabetes: effects of insulin, vascular risk factors and blood-glucose levels. European Journal of Pharmacology. 2004;490(1–3):159–168. - PubMed
    1. Russell JW, Golovoy D, Vincent AM, et al. High glucose-induced oxidative stress and mitochondrial dysfunction in nuerons. The FASEB Journal. 2002;16(13):1738–1748. - PubMed
    1. Tayarani I, Chaudiere J, Lefauconnier J-M, Bourre J-M. Enzymatic protection against peroxidative damage in isolated brain capillaries. Journal of Neurochemistry. 1987;48(5):1399–1402. - PubMed

LinkOut - more resources