No abstract

Multiple sclerosis (MS) is a demyelinating chronic autoimmune inflammatory disease of the central nervous system (CNS). A large amount of proinflammatory cytokines is released in the CNS from the self-reactive T cells infiltrate, leading to the destruction of the myelin sheath and contributing to the development of MS. Several drugs have emerged in recent years to treat MS, and studies have shown that gold nanoparticles (GNPs) have anti-inflammatory properties in autoimmune diseases. Thus, the effects of GNP conjugation to ethylene dicysteine diethyl ester (ECD) were evaluated in C57BL/6 female mice exposed to experimental MS. Animals were exposed to experimental autoimmune encephalitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG35-55) in complete Freund’s adjuvant supplemented with Mycobacterium tuberculosis. The clinical and cerebral effects of the different doses of ECD–GNPs (0.3, 0.6, and 1.0 mg/kg) were first studied, and the results showed that the group treated with 0.6 mg/kg ECD–GNPs improved clinical symptoms, inflammatory infiltrate, and myelin integrity. In the following step, GNPs and ECD–GNPs (0.6 mg/kg) showed improvements in the clinical signs of the disease. Moreover, there was a reduction in the levels of proinflammatory cytokines in both groups compared to EAE, and only the isolated use of GNPs increased IL-4 expression. Both NF-κB and TGFβ immunoexpression were significantly reduced following EAE + GNPs and EAE + ECD–GNPs treatment. In conclusion, GNPs and ECD–GNPs at 0.6 mg/kg attenuate the neurological signs of EAE likely due to inhibition of neuroinflammation induced by EAE.

Glioblastoma is a very aggressive and common brain cancer. Previous studies have shown that changes in the brain's redox biology interfere with behavioral patterns and DNA damage. The results of these studies, however, have been inconclusive. To evaluate the effects of a physical training program on behavioral aspects, redox and genomic stability parameters in animals exposed to an experimental model of GBM. Forty-seven male C57BL/6J mice aged sixty days were randomly selected and divided into two groups (GBM and sham/placebo surgery), which were subsequently divided into four groups: untrained sham (Sut, n = 10), untrained GBM (Gut, n = 15), trained sham (Str, n = 10), and trained GBM (Gtr, n = 12). The trained animals performed 3 sessions, followed by a rest day, of moderate aerobic exercise on a treadmill for four consecutive weeks, while the untrained animals were kept in boxes during the experimental period. Behavioral indicators were evaluated with open field and rota rod tests. After the last training session, the animals were euthanized and brain, liver, bone marrow, and blood were collected for analysis of redox and genomic instability markers. The results showed higher latency values were sustained by the exercise in Gtr. The elevated levels of total reactive oxygen species in the parietal tissue of Gut animals were reversed after physical training. The Gtr group had a lower tail intensity. Physical exercise is a promise as an adjunctive therapy for the management of GBM by modulating redox parameters in the parietal tissue and reduces the genomic instability in liver and blood.