Abstract
Sevoflurane is a commonly utilized inhalational anesthetic in surgical settings. Nevertheless, sevoflurane has been demonstrated to possess neurotoxic properties. The objective was to examine the neuroprotective function of long non-coding RNA prostate androgen-regulated transcript 1 (PART1) in sevoflurane-induced neurotoxicity and to elucidate its potential mechanism. The level of PART1 was quantified by RT-qPCR. The proliferation and apoptosis of HT22 cells were evaluated through CCK-8 assay and flow cytometry, respectively. To assess the protein level of IL-6, IL-1β, and TNF-α, ELISA was conducted. The levels of malondialdehyde, nitrite, and reduced glutathione along with the activity of superoxide dismutase were determined to evaluate oxidative stress. Verification of the targeting relationship between miR-16-5p and PART1 was performed using the dual-luciferase reporter assay. The Morris water maze test was used to assess the impact of PART1 on sevoflurane-induced learning and cognitive function in rats. PART1 levels were decreased in sevoflurane-treated HT22 cells and rats. PART1 suppressed sevoflurane-induced apoptosis and attenuated its inhibitory effect on cell proliferation. PART1 mitigated sevoflurane-induced inflammatory response and oxidative stress in HT22 cells through the regulation of miR-16-5p. PART1 suppressed oxidative damage and inflammatory response leading to improvement of learning and cognitive function in rats subjected to sevoflurane exposure. PART1 has the potential to regulate the sevoflurane-induced inflammatory response and oxidative stress via miR-16-5p, which in turn improves learning and cognitive function. Consequently, PART1 may be a promising therapeutic target for sevoflurane-induced neurotoxicity.