To investigate the mechanism dexmedetomidine in relieving the neurotoxicity of a developing brain induced by sevoflurane. Sprague-Dawley rats, 6 days old, were randomly divided into three groups. Rats in the control group were inhaled with air after injection of normal saline; rats in the sevoflurane group were injected with normal saline and inhaled with 3% sevoflurane for 2 h in three consecutive day; rats in the dexmedetomidine group were inhaled with 3% sevoflurane after intraperitoneal injection of dexmedetomidine 25 μg/kg. WB results showed that mBDNF, pTrkB/TrkB, and CREB were significantly decreased in the hippocampus of the sevoflurane group, which are significantly upregulated in the dexmedetomidine group. In the sevoflurane group, proBDNF, P75NRT, and RhoA were significantly increased, which were significantly lower than those in the dexmedetomidine group than those in the sevoflurane group. The expression BDNF was downregulated in the sevoflurane group, while the proBDNF was upregulated in the sevoflurane group. In the Morris water maze test, the escape latency of the sevoflurane group was significantly prolonged. In sevoflurane groups, the number of crossing platform was significantly reduced, the synaptic protein decreased significantly, and this effect was reversed in rats of the dexmedetomidine group. Dexmedetomidine could reduce synaptic plasticity decline in developing rats induced by sevoflurane, through downregulating the proBDNF-p75NTR-RhoA pathway and upregulating BDNF-TrkB-CREB.

中文翻译：

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右美托咪定通过上调BDNF-TrkB-CREB和下调ProBDNF-P75NRT-RhoA信号通路来减轻七氟醚所致发育中大鼠的神经毒性。

为了研究右美托咪定缓解七氟醚诱导的发育中脑神经毒性的机制。将6天大的Sprague-Dawley大鼠随机分为三组。对照组在注射生理盐水后吸入空气。七氟醚组大鼠连续三天注射生理盐水并吸入3％七氟醚2 h。大鼠右美托咪组中右美托咪25的腹膜内注射后，用3％的七氟醚吸入 μ克/千克 WB结果显示，七氟醚组海马中的mBDNF，pTrkB / TrkB和CREB显着降低，而右美托咪定组则显着上调。在七氟醚组中，proBDNF，P75NRT和RhoA显着增加，这明显低于右美托咪定组的水平。七氟醚组中BDNF的表达下调，而七氟醚组中proBDNF的表达上调。在莫里斯水迷宫测试中，七氟醚组的逃避潜伏期显着延长。在七氟醚组中，交叉平台的数量显着减少，突触蛋白显着降低，在右美托咪定组的大鼠中这种作用被逆转。