Anesthetic Model MicroRNA Main Findings Reference
Propofol Human embryonic stem cell-derived neurons miR-21 The expression of miR-21 was downregulated following exposure to 6 hours of 20 µg/mL propofol. Overexpression of miR-21 attenuated the propofol-induced cell death. The toxicity occurred through a STAT3/miR-21/Sprouty 2/Akt-dependent mechanism. Twaroski, et al.[45]
         
Ketamine Neonatal mice miR-34c miR-34c was upregulated in the hippocampus of neonatal mice exposed to ketamine and downregulation of miR-34c attenuated the ketamine-induced neuronal cell death and cognitive impairment observed in the animals. Cao, et al.[72]
         
Ketamine Neonatal mice miR-124 miR-124 was upregulated in the hippocampus of neonatal mice exposed to ketamine and knockdown of miR-124 reduced ketamine-induced apoptosis in hippocampal CA1 neurons in vitro and activated the PKC-ERK pathway. miR-124 knockdown improved memory performance of mice treated with ketamine. Xu, et al.[73]
         
Ketamine One-month old C57/BL6 mice miR-34a Exposure to 50 mg/kg ketamine for 7 days induced apoptosis in hippocampal CA1 neurons and upregulated hippocampal miR-34a. Inhibition of miR-34a protected against anesthesia-induced neuroapoptosis and memory impairment while knockdown of its target, FGFR1 exacerbated the toxicity. Jiang, et al.[74]
         
Ketamine One-month old Sprague-Dawley rats miR-137 Exposure to 75 mg/kg ketamine for 3 days induced apoptosis in hippocampal CA1 neurons, downregulation of miR-137 in the hippocampus, and long-term memory impairment. Overexpression of miR-137 protected against hippocampal neurodegeneration and memory loss. Huang, et al. [75]
Table 2: Studies depicting a role of microRNAs in anesthetic-induced developmental neurotoxicity