INTRODUCTION: Substantial evidence has indicated that isoflurane leads to learning and memory impairment. This study was designed to investigate the potential role of microRNA-124-3p (miR-124-3p) in isoflurane-induced learning and memory impairment in rats. METHODS: Spatial learning and memory of rats were estimated by the Morris water maze (MWM) test after the construction of isoflurane-treated models. qRT-PCR was performed to assess the expression levels of miR-124-3p. The levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α in the hippocampal tissues were determined by enzyme-linked immunosorbent assay. The luciferase activity was determined by using a dual-luciferase reporter assay system. RESULTS: The higher escape latency and lower time spent in the original quadrant were shown in isoflurane-treated rats compared with the control rats. Moreover, treatment with isoflurane could induce neuroinflammation, and miR-124-3p was poorly expressed in the hippocampal tissue of isoflurane-treated rats. Furthermore, STAT3 is a functional target of miR-124-3p, and inflammatory cytokine level was downregulated by miR-124-3p. DISCUSSION/ CONCLUSION: Combining the results of the current study demonstrates that miR-124-3p may have pivotal roles in improving isoflurane-induced learning and memory impairment via targeting STAT3 and inhibiting neuroinflammation.
INTRODUCTION: Substantial evidence has indicated that isoflurane leads to learning and memory impairment. This study was designed to investigate the potential role of microRNA-124-3p (miR-124-3p) in isoflurane-induced learning and memory impairment in rats. METHODS: Spatial learning and memory of rats were estimated by the Morris water maze (MWM) test after the construction of isoflurane-treated models. qRT-PCR was performed to assess the expression levels of miR-124-3p. The levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α in the hippocampal tissues were determined by enzyme-linked immunosorbent assay. The luciferase activity was determined by using a dual-luciferase reporter assay system. RESULTS: The higher escape latency and lower time spent in the original quadrant were shown in isoflurane-treated rats compared with the control rats. Moreover, treatment with isoflurane could induce neuroinflammation, and miR-124-3p was poorly expressed in the hippocampal tissue of isoflurane-treated rats. Furthermore, STAT3 is a functional target of miR-124-3p, and inflammatory cytokine level was downregulated by miR-124-3p. DISCUSSION/ CONCLUSION: Combining the results of the current study demonstrates that miR-124-3p may have pivotal roles in improving isoflurane-induced learning and memory impairment via targeting STAT3 and inhibiting neuroinflammation.