目的：观察丙泊酚预处理在脂多糖（LPS）诱导的脓毒血症小鼠抑郁样行为和海马炎症反应中的作用， 并探讨其可能的作用机制。方法：60只健康ICR小鼠随机分为6组：对照组（C组），丙泊酚组（P1组），LPS组 （L5组），丙泊酚+LPS组（L5P1、L5P2、L5P5组），每组10只。P1组注射10 mg/kg丙泊酚；L5组注射5 mg/kg LPS；L5P1 组、L5P2 组和 L5P5 组分别注射 10 mg/kg、20 mg/kg 和 50 mg/kg 丙泊酚预处理，30 min 后注射 5 mg/kg LPS。所有药物均选择腹腔注射，C组注射同等剂量的生理盐水。24 h后依次采用糖水偏好实验、 悬尾实验和强迫游泳实验对小鼠进行抑郁样行为测试；行为学测试后处死小鼠，采用免疫印迹法检测脑炎 性因子Toll样受体4（TLR4）、核转录因子κB（NF-κB）主要蛋白P65、髓样分化因子-2（MD-2）表达水平。结 果：与C组比较，L5组糖水摄取量减少，悬尾静止时间延长，TLR4、P65、MD-2表达量升高（P＜0.05）。与L5 组比较，L5P1组糖水摄取量增加，TLR4、P65、MD-2表达量降低（P＜0.05）；L5P2组糖水摄取量增加，悬尾静 止时间缩短，P65、MD-2表达量降低（P＜0.05）；L5P5组糖水摄取量增加，P65表达量降低（P＜0.05）。结论： 丙泊酚预处理可改善LPS诱导的脓毒血症小鼠抑郁样行为，降低海马炎症因子的表达，这可能与丙泊酚抑 制TLR4/MD-2通路，减轻炎症反应有关。

To observe the effect of propofol pretreatment on the depression-like behavior and hippocampal inflammatory response of lipopolysaccharide (LPS)-induced sepsis in mice and to explore its possible mechanism. Methods: Sixty healthy ICR mice were randomly devided into six groups (n=10): control group (group C), propofol group (group P1), LPS group (group L5), and propofol + LPS groups (groups L5P1, L5P2, and L5P5). Sepsis was induced in mice by injection with 5 mg/kg LPS. Group P1 was injected with 10 mg/kg propofol. Group L5P1, group L5P2, and group L5P5 were injected with 10 mg/kg, 20 mg/kg, and 50 mg/kg propofol, respectively. After 30 minutes, mice were injected with 5 mg/kg LPS. Group C was injected with the same amount of normal saline. All injections were intraperitoneal. After 24 hours, the depression-like behavior of mice was tested by the sucrose preference test, tail suspension test, and forced swimming test. Mice were sacrificed after behavior tests; subsequently, the expression level of inflammatory factors TLR4, P65 (main protein in NF-κ B), and MD-2 were detected by Western blot. Results: Compared with group C, group L5 showed decreased sucrose intake, increased tail suspension time, and inceased expression of TLR4, P65, and MD-2 (P<0.05). Compared with group L5, group L5P1 showed increased sucrose intake and reduced expression of TLR4, P65, and MD-2 (P<0.05); group L5P2 showed decreased sucrose intake, decreased tail suspension time, and reduced expression of P65 and MD-2 (P<0.05); group L5P5 showed increased sucrose intake and reduced expression of P65 (P<0.05). Conclusion: Propofol can improve the depression-like behavior and reduce the expression of hippocampal inflammatory factors in LPS-induced sepsis in mice. The mechanism may be related to inhibiting the TLR4/MD-2 pathway and reducing inflammatory responses.