Background and Objective: Sevoflurane is known to be associated with cognitive impairment during anesthesia in Alzheimer's Disease (AD) patients. However, the molecular mechanism underlying the pathogenesis caused by sevoflurane-induced anesthesia is not properly understood. The present investigation was an attempt to understand the molecular mechanism of sevoflurane anesthesia in causing cognitive decline in AD patients using aged rats as the model organism. Materials and Methods: In this study, aged rats (n = 60) were categorized into six different groups (CON, SLF-0, SLF-2, SLF-4, SLF-6 and SLF-8) having a population size of 10 rats in each group. The Control (CON groups were given 40% O2 for 2 h) and the SLF groups were placed under anesthesia with 2.2% sevoflurane and 30% O2 for 60 min. The rats in each of the SLF groups were analyzed for the exposure. The MWM (Morris water maze) test was assessed for assessing the cognitive function of the aged rats and the expression level of APP (Amyloid Precursor Protein), BACE-1 (beta-site APP Cleavage Enzyme-1) and A beta 42 (Beta-amyloid-42) oligomers were analyzed compared to the CON group. Results: The study observed that the protein expression levels of APP mRNA were increased because of sevoflurane-induced anesthesia thereby promoting the overproduction of A beta 42 oligomers and depletion of APP protein. Interestingly, the expression of BACE-1 was not affected. Moreover, the SLF groups showed an increase in the escape latency and impaired memory. Conclusion: The study suggested that sevoflurane-induced anesthesia contributed to the cognitive decline in aged rats due to had increased expression of APP mRNA and oligomerization of A beta 42 peptide.
[1]Jilin Univ, Dept Obstet & Gynecol, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China.
[2]Jilin Univ, Dept Anesthesiol, China Japan Union Hosp, Changchun 130033, Jilin, Peoples R China.
(8.0+极速模式)