七氟烷吸入麻醉通过激活大鼠的炎症和细胞凋亡途径来改变认知功能
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Sevoflurane anesthesia alters cognitive function by activating inflammation and cell death in rats
背景与目的
本研究旨在讨论七氟醚吸入麻醉对大脑认知功能的影响，并探讨介导这种作用的分子机制。
方 法
将100只健康雄性Sprague-Dawley大鼠分成四组：i）对照组（空气吸入），ii)低剂量组（1.5％七氟烷吸入2小时），iii）高剂量组（3％七氟烷吸入2小时）和iv）尼莫地平组（3％七氟烷吸入2小时+尼莫地平）。
结 果
七氟烷吸入麻醉以剂量依赖性方式导致认知功能障碍。七氟烷还可以上调海马体内肿瘤坏死因子—α（TNF-α）,白细胞介素（IL）-6，-8和半胱天冬梅-3的表达。尼莫地平干预部分恢复了七氟烷诱导的认知功能及TNF-α，IL-6，IL-8和Caspase-3的异常表达。
结 论
结果表明，七氟烷吸入麻醉导致大鼠认知功能障碍可能与炎症和凋亡途径的激活有关。尼莫地平的神经保护作用表明异常的钙转运是七氟烷毒性的部分原因。
原始文献摘要
Cui R S, Wang K, Wang Z L. Sevoflurane anesthesia alters cognitive function by activating inflammation and cell death in rats[J]. Experimental & Therapeutic Medicine, 2018.
Objective
The present study was designed to investigate the effects of sevoflurane inhalation anesthesia on the cognitive function of rats and to investigate the molecular mechanisms mediating this effect.
Methods
A total of 100 healthy male Sprague-Dawley rats were divided into four groups: i) Control (air inhalation), ii) low-dose (1.5% sevoflurane inhalation for 2 h), iii) high‑dose (3% sevoflurane inhalation for 2 h), and iv) nimodipine group (3% sevoflurane inhala[1]tion for 2 h + nimodipine).
Results
Sevoflurane inhalation anesthesia resulted in cognitive dysfunction in a dose-dependent manner. Sevoflurane also upregulated the expression of tumour necrosis factor-α (TNF-α), interleukin (IL) -6, -8, and Caspase-3 in the hippocampus. The intervention with nimodipine partially recovered the cognitive function and the abnormal expression of TNF-α, IL-6, IL-8, and Caspase-3 induced by sevoflurane..
Conclusions
The results showed that the cognitive dysfunction caused by sevoflurane inhalation in rats may be related to the activation inflammatory and apoptotic pathways. The neuroprotective effect of nimodipine suggests that abnormal calcium transport is partially responsible for the sevoflurane toxicity.
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