MicroRNAs-Based Theranostics against Anesthetic-Induced Neurotoxicity

Abstract

Various clinical reports indicate prolonged exposure to general anesthetic-induced neurotoxicity (in vitro and in vivo). Behavior changes (memory and cognition) are compilations commonly cited with general anesthetics. The ability of miRNAs to modulate gene expression, thereby selectively altering cellular functions, remains one of the emerging techniques in the recent decade. Importantly, engineered miRNAs (which are of the two categories, i.e., agomir and antagomir) to an extent found to mitigate neurotoxicity. Utilizing pre-designed synthetic miRNA oligos would be an ideal analeptic approach for intervention based on indicative parameters. This review demonstrates engineered miRNA’s potential as prophylactics and/or therapeutics minimizing the general anesthetics-induced neurotoxicity. Furthermore, we share our thoughts regarding the current challenges and feasibility of using miRNAs as therapeutic agents to counteract the adverse neurological effects. Moreover, we discuss the scientific status and updates on the novel neuro-miRNAs related to therapy against neurotoxicity induced by amyloid beta (Aβ) and Parkinson’s disease (PD).

Unraveling the signaling network between dysregulated microRNA and mRNA expression in sevoflurane-induced developmental neurotoxicity in rat

“…Furthermore, the transient cellular and molecular changes triggered by sevoflurane toxicity can exert long-lasting effects on behavior and function. Moreover, just as the transient cellular and molecular changes triggered by sevoflurane toxicity can exert long-lasting effects on behavior and function, the miRNA-mRNA network and its corresponding pathways are likely to be upregulated or downregulated at different developmental stages, which may contribute to the progression of neurotoxicity [ [26] , [27] , [28] ]. Based on our data, we identified 5 miRNAs (rno-miR-449a-3p, rno-miR-449c-5p, rno-miR-652-5p, rno-miR-130b-5p, rno-miR-451-5p) and 44 putative dysregulated mRNAs in the hippocampal tissue of rats after sevoflurane exposure.…”