Nombre: BEATRIZ NUNES SANTOS
Fecha de publicación: 10/04/2025
Junta de examinadores:
Nombre |
Papel |
|---|---|
| CARMEM LUIZA SARTÓRIO | Examinador Externo |
| EVANDRO MANOEL NETO NEVES | Examinador Interno |
Sumario: Traumatic brain injury (TBI) and its sequelae are responsible for a large portion of
trauma-related deaths worldwide. Due to its complex pathophysiology, many
post-injury processes are still poorly understood. The secondary injuries occur
mainly due to mechanisms such as excitotoxicity, which facilitates oxidative stress
and neuroinflammation processes, leading to cognitive and psychiatric impairment.
Animal models allow for a better understanding of the progression of TBI, as well as
enabling the search for effective therapies for secondary injuries. The weight-drop
model simulates, in rodents, a trauma that closely resembles human TBI. Despite
there being no effective therapeutic for secondary TBI damage to date, studies on the
effectiveness of N-acetylcysteine (NAC) in various other conditions, from neurological
to psychiatric, have gained notoriety. NAC exhibits significant antioxidant and
anti-inflammatory activity that may be associated with neuroprotection and is a
low-cost substance with no relevant side effects. Therefore, this project aims to
elucidate the effects of NAC on behavioral and oxidative stress in young adult rats
subjected to the weight-drop model of TBI. A total of 121 Wistar rats were used,
divided into six groups: Sham-Vehicle, Sham-NAC 150 mg/kg, Sham-NAC 300
mg/kg, TBI-Vehicle, TBI-NAC 150 mg/kg, and TBI-NAC 300 mg/kg. The animals
were subjected to open field and object recognition behavioral tests, and the
evaluation of oxidative stress was carried out using the AOPP and TBARs assays.
As main results, the animals treated with both NAC doses showed better
performance in mobility assessed by the open field, a higher recognition index in
long-term memory assessed by the novel object recognition, and lower oxidative
stress in AOPP and TBARs. Thus, it is suggested that NAC may be a great ally in
the treatment of secondary damage caused by TBI.
