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Expression and Significance of Cdc42 in the Hippocampus Rat Tissue Caused by Sevoflurane Neurotoxicity |
HAN Tao, CHEN Qin |
Hunan Provincial Maternal and Child Health Care Hospital,Hunan Changsha 410006 |
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Abstract 【Objective】 The aim of this study is to explore the expression and significance of Cdc42 (cell division cyclin42) in the hippocampus tissue of rats with neurotoxicity of sevoflurane. 【Methods】 Forty-two Sprague Dawley (SD) rats of 7 days old were randomly divided into three groups (n=14): group A, group B and group C. Rats in group A were exposed to 2% sevoflurane and 80% oxygen inhalation once for 2 hours. Rats in group B were exposed to 2% sevoflurane and 80% oxygen inhalation 2 hours/day for three consecutive days. Rats in group C received only 80% oxygen inhalation for 2 hours. Rats were sacrificed at 3 hours after experimental models completed and the hippocampus tissues were collected to measure the expression of Cdc42 and cleaved caspase3 (cysteine proteolytic enzyme 3, CI-Csp3) by western blot. Spatial learning and memory ability of adult rats were detected by Morris water maze (MWM) test at 45-49 days after birth. 【Results】 Compared to the group C, the expression of Cdc42 and Cl-Csp3 in the hippocampus of the group A had no significant difference (P>0.05), whereas the expression of Cdc42 and Cl-Csp3 in the hippocampus of group B increased significantly (P<0.05). In place navigation test, there was no significant difference of the escape latency between group C and group A (P>0.05). The escape latency of rats in the group B were significantly longer than that of C group (P<0.05). In probe trial test, the percent time in target quadrant in group A was not different from that of group C (P>0.05), While the percent time in target quadrant in group B decreased (P<0.05). 【Conclusion】 Multiple inhalation of sevoflurane can induce neurotoxicity and memory dysfunction, which may be related to the increase in the expression of Cdc42.
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Received: 25 August 2020
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