| 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] |
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| 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] |
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| 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] |
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| 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] |
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| 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] |