Abstract:Objective To investigate the effect of isoflurane inhalation anesthesia on perioperative neurocognitive function of mice and the mechanism. Methods C57BL/6 mice were randomly divided into the control group, 2% isoflurane group, surgery group and 2% isoflurane + surgery group, with 20 mice in each. Morris water maze test was used to evaluate the cognitive function of mice one, three and seven days after surgery. The levels of inflammation and apoptosis related factors in the hippocampus were measured. The activation of astrocytes was observed with immunofluorescence staining while apoptosis was detected by TUNEL. Results Compared with the 2% isoflurane group and surgery group, the escape latency [(77.36±13.48)s vs. (66.71±4.54)s, (64.47±4.43)s],[(51.63±8.43)s vs. (46.37±5.69)s, (45.72±5.71)s],[(30.85±4.56)s vs. (21.13±3.24)s, (22.36±3.18)s] of the 2% isoflurane + surgery group was significantly increased one, three and seven days after operation, while the time spent in the target quadrant[(13.16±4.25)s vs. (35.36±4.48)s, (36.14±4.42)s],[(19.48±6.37)s vs. (37.64±6.33)s, (37.15±6.28)s], [(23.69±5.54)s vs. (39.15±6.34)s, (38.63±5.43)s] was significantly shortened. The expression of TNF-α in the hippocampus was significantly decreased, while the expressions of IL-6 and caspase-3 were significantly increased. The number of GFAP positive cells [(11.97±1.35) vs. (14.15±1.48), (15.67±1.51)], [(34.74±1.52) vs. (31.92±1.44), (31.96±1.52)],[(35.69±1.48) vs. (32.14±1.51), (31.96±1.52)] and the apoptosis rate of hippocampal neurons [(56.71±1.87)% vs. (48.63±1.45)%, (48.34±1.69)%],[(59.64±1.57)% vs. (49.63±1.51)%, (49.45±1.58)%],[(63.49±2.62)% vs. (50.68±2.45)%, (50.38±2.44)%] were significantly increased (P<0.05). Conclusions Isoflurane inhalation anesthesia can cause the decline of cognitive function in perioperative mice, and the mechanism may be related to promoting the activation of hippocampal astrocytes, inducing neuronal apoptosis and aggravating the level of neuroinflammation.
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