Neuroprotective Effects Of N-Acetylcysteine (Nac) Against Memory Disorders Which Is Induced By Sleep Deprivation (Sd): Experimental Research On Young Rats

In this study, to obtain young SD model rats, the rats were treated by being placed on the SD platform for three days. We observed that rats that experienced sleep deprivation (SD) using the multiple platform method did not show significant changes in body weight compared to the control group. This finding indicates that physical stress induced by the SD method did not significantly affect the body weight of the rats.in our study, no significant weight loss was found. This difference may be due to the shorter duration of SD. This suggests that the multiple platform method for SD induction does not always cause significant weight changes in mice, depending on various factors such as the duration of SD and the characteristics of the study subjects.

This study also explored the relationship between ACh, AChE activity, and NAC in the context of cognitive dysfunction caused by SD. ACh and AChE are two important components in cholinergic neurotransmission that play a major role in memory processes. SD is known to have a negative impact on the cholinergic system, which can directly affect memory and learning functions. (58) The results showed that there was a tendency for increased AChE activity in the hippocampus in the SD group compared to normal, although not significant. Based on several previous studies, it takes a longer time to increase AChE activity in the hippocampus with SD treatment, including 21 days in mice, (103) and 45 days in rats. (104) This increase in AChE activity causes a decrease in ACh levels, which is an important neurotransmitter for cognitive and memory processes. (58).

This study also aims to assess the role of IL-1β, TNF-α, and NLRP3 in the brain inflammatory response induced by SD. SD is known to increase inflammation in the brain through increased expression of pro-inflammatory cytokines such as IL-1B and TNF-α. Inflammation that occurs in SD can cause impaired memory function and neurodegeneration. (59, 107) The results showed that SD significantly increased mRNA expression of TNF-α in the prefrontal cortex, but did not increase IL-1β. TNF-α is produced more rapidly in the early phase of the inflammatory response. TNF-α production begins with the recognition of inflammatory stimulation by receptors, which triggers the activation of NF-κB and MAPK, which will increase TNF-α gene expression. As for IL-1β, it takes longer to be produced. IL-1β is produced in an inactive form as 65 pro-IL-1β and is then processed into the active form by the caspase-1 enzyme which is usually activated via the inflammasome (especially NLRP3).(108, 109).

The results of the study showed that in SD there was a tendency to decrease neuron density in the hippocampus, as seen from the results of NADPH diaphorase staining. Previous studies have shown that SD increases oxidative stress and 67 increases NO, which contributes to neuron damage. (114, 115) NO produced by NOS has an important role in neuroplasticity and memory processes. NAC administration also tends to increase hippocampal neuron density. This is in line with several studies showing that NAC reduces excessive NO production which can cause neurodegeneration through the formation of ROS and RNS species. (116, 117).