MOLECULAR ANALYSIS OF GENE EXPRESSION IN WISTAR RATS SUBMITTED TO INTRACEREBROVENTRICULAR STREPTOZOTOCIN (STZ-ICV) AND EXPERIMENTAL TREATMENT WITH DIMETHYL SULFOXIDE (DMSO)

• DOI: 10.22533/at.ed.1593132318023

• Palavras-chave: -

• Keywords: Alzheimer disease. Dimethyl sulfoxide. Streptozotocin.

• Abstract:

  Alzheimer disease represents the most frequent neurodegenerative and
  prevalent process in the adult population related to genetic and environmental
  factors, with no curative treatment even with current technological innovations. Thus,
  it is important to search for therapeutic proposals that minimize or even interrupt
  the neurodegenerative processes common of the disease. Dimethyl sulfoxide
  (DMSO) has high molecular versatility, with a potential neuroprotective effect.
  Neurodegeneration induced by intracerebroventricular streptozotocin (STZ-icv) in
  rodents leads to a neuropathological phenotype similar to sporadic Alzheimer
  disease. The aim of this study was to assess the potential neuroprotective effect of
  DMSO on memory impairments induced by STZ in Wistar rats, with molecular

  2

  analyses performed by hippocampal extraction through qPCR and assessing the
  expression profile of genes related to neuroinflammation (interleukin 1β; IL 1-β, tumor
  necrosis factor-α: TNF-α), reactive species of mitochondrial oxidative stress; catalase
  (CAT), and an activator of adulthood neurogenesis (brain-derived neurotrophic
  factor; BDNF), where a trend in reduction of neuroinflammation was observed
  through lower expression of IL1-β, TNFα, mitochondrial oxidative stress with
  degradation of CAT in the scavenging of reactive oxygen species, and an increase in
  the expression of BDNF at the dose of 1.5 g/kg DMSO in the treatment group, related
  to a cellular environment favourable to neuroprotection and cell survival upon
  induction of neurodegeneration.