Background. Propofol (PPF) has been shown in studies to cause cognitive impairment and neuronal cell death in developing animals. PPF has been demonstrated to decrease the expression of microRNA-17-5p (miR-17-5p) in a recent study. Nonetheless, the function of miR-17-5p in PPF-induced neurotoxicity and related mechanisms is uncharacterized. Methods. After the induction of neurotoxicity by treating the SH-SY5Y cells with PPF, qRT-PCR was conducted to evaluate the level of miR-17-5p. Using MTT and flow cytometry, cell viability and apoptosis rate were assessed, respectively. Interaction between miR-17-5p and BCL2 like 11 was (BCL2L11) studied using a Luciferase reporter assay. With the help of western blot analysis, we determined the level of proteins of apoptosis-related genes and autophagy-related markers. Results. In SH-SY5Y cells, PPF treatment induced neurotoxicity and downregulated miR-17-5p expression. In SH-SY5Y cells post-PPF exposure, overexpression of miR-17-5p increased cell viability and decreased apoptosis. Consistently, miR-17-5p mimics mitigated PPF-generated autophagy via inhibition of Atg5, Beclin1, and LC3II/I level and elevation of p62 protein expression. In addition, BCL2L11, which was highly expressed in PPF-treated SH-SY5Y cells, was directly targeted by miR-17-5p. Further, in PPF-treated SH-SY5Y cells, overexpressed BCL2L11 counteracted the suppressing behavior of miR-17-5p elevation on PPF-induced apoptosis. Conclusion. Overexpressed miR-17-5p alleviates PPF exposure-induced neurotoxicity and autophagy in SH-SY5Y cells via binding to BCL2L11, suggesting the possibility that miR-17-5p can serve as a candidate in the treatment of neurotoxicity (caused by PPF).

Isoflurane (ISO) is a type of anesthetic that might cause neurotoxicity in children. Although miR-424-5p is considerably downregulated in ISO-treated rat brain samples, its physiological role in ISO-induced neuronal injury in human embryonic stem cell-derived neurons remains unknown (hESC-derived neurons). miR-424-5p expression and fatty acid synthase (FASN) in ISO-treated hESC-derived neurons were tested via qRT-PCR. The amount of protein for Bax, Cleaved-caspase-8, Bcl-2, and FASN was investigated through western blot analysis. The viability and apoptosis of hESC-derived neurons were estimated through cell counting kit-8 assessment and TUNEL assay, accordingly. Superoxide dismutase, glutathione, and malondialdehyde levels were discovered via corresponding kits. The contents of inflammatory factors including interleukin-6 and tumor necrosis factor-α were examined by enzyme-linked immunosorbent assays. The combination between FASN and miR-424-5p was resolute via dual-luciferase reporter assessment. After exposure to ISO, induced neurotoxicity and a decreased miR-424-5p production were identified in hESC-derived neurons. Upregulation of miR-424-5p repressed ISO-induced apoptosis and mitigated ISO-induced inflammatory response and oxidative stress in vitro. FASN expression levels were reduced by elevation of miR-424-5p and upregulated after ISO treatment. Mechanically, FASN was directly targeted by miR-424-5p in hESC-derived neurons. Of note, the miR-424-5p elevation-suppressed neuronal apoptosis, inflammatory response, and oxidative stress were countered by upregulation of FASN.