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目的:研究松花粉对脂多糖（LPS）诱发小鼠学习记忆功能损伤的保护作用和机制。方法:将60只小鼠采用数字表法随机分为四组：正常对照组（n n=15）、模型组（n n=15）、松花粉低剂量组（500 mg/kg，n n=15）和松花粉高剂量组（1 000 mg/kg，n n=15）。小鼠侧脑室一次性注射LPS建立小鼠学习记忆功能损伤模型，通过水迷宫实验检测小鼠的学习记忆能力，同时测定小鼠海马超氧化物歧化酶（SOD）的活性，谷胱甘肽（GSH）和丙二醛（MDA）的含量，同时检测小鼠海马白细胞介素6（IL-6）、肿瘤坏死因子α（TNF-α）含量，以及多巴胺（DA）和去甲肾上腺素（NE）的含量。n 结果:与正常对照组小鼠相比，模型组小鼠避暗实验潜伏期［（134.80±33.89）s比（282.20±17.43）s］明显缩短（n t=4.23，n P<0.01），错误次数［（4.00±1.58）次比（1.20±1.30）次］显著升高（n t=2.85，n P<0.01）。给予松花粉治疗后可显著提升小鼠避暗实验潜伏期［（189.40±27.21）s、（213.40±21.26）s比（134.80±33.89）s］（n t=3.21、4.38，均n P<0.05），降低小鼠的错误次数［（1.60±1.44）次、（1.40±1.44）次比（4.00±1.58）次］（n t=5.12、6.42，均n P<0.05）。同时，模型组小鼠海马中SOD的活性，GSH、DA、NE的含量较正常对照组小鼠［（7.59±1.77）kU/g比（39.90±6.37）kU/g，（3.49±0.13）mmol/g比（6.37±0.14）mmol/g，（418.42±2.57）ng/L比（586.37±3.64）ng/L，（187.20±5.41）ng/L比（298.42±2.32）ng/L］显著降低（n t=3.67、8.23、2.23、3.65，均n P<0.05），MDA、IL-6和TNF-α的含量［（8.79±0.82）mmol/g比（2.62±0.16）mmol/g，（48.07±5.56）ng/L比（18.76±1.42）ng/L，（87.20±4.31）ng/L比（22.42±3.39）ng/L］显著升高（n t=7.45、2.67、4.35，n P<0.05或n P<0.01）。给予松花粉治疗后，与模型组小鼠相比，SOD的活性，GSH、DA和NE的含量［（18.80±2.39）kU/g、（28.70±2.36）kU/g比（7.59±1.77）kU/g，（5.04±0.36）mmol/g、（5.45±0.17）mmol/g比（3.49±0.13）mmol/g，（488.37±3.46）ng/L、（506.29±5.72）ng/L比（418.42±2.57）ng/L，（225.65±3.72）ng/L、（239.76±5.58）ng/L比（187.20±5.41）ng/L］显著升高（n t=4.56、6.71，n t=4.65、5.32，n t=4.73、6.72，n t=3.84、5.63，n P<0.05或n P<0.01），MDA、IL-6和TNF-α的含量［（5.72±0.47）mmol/g、（3.77±0.23）mmol/g比（8.79±0.82）mmol/g，（28.42±3.54）ng/L、（23.43±5.62）ng/L比（48.07±5.56）ng/L，（48.87±4.82）ng/L、（39.65±6.69）ng/L比（87.20±4.31）ng/L］显著降低（n t=6.31、7.28，n t=3.46、6.31，n t=4.28、3.57，n P<0.05或n P<0.01）。n 结论:松花粉对LPS诱导的小鼠学习记忆能力损伤具有改善作用，其作用机制可能与其上调小鼠海马中单胺类神经递质DA和NE的水平，以及抑制海马氧化应激和炎性反应水平有关。“,”Objective:To investigate the protective effect of pine pollen on lipopolysaccharide (LPS)-induced learning and memory impairments in mice and the underlying mechanism.Methods:Sixty mice were randomly divided into four groups (n n = 15/group): normal control, model, low-dose pine pollen (500 mg/kg) and high-dose pine pollen (1 000 mg/kg). Mouse models of learning and memory impairment were established by lateral ventricle injection of LPS. The learning and memory abilities of mice were determined by the Morris water maze test. Superoxide dismutase (SOD) activity and glutathione (GSH) and malondialdehyde (MDA) levels in the hippocampus of mice were measured. Interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), dopamine (DA), and norepinephrine (NE) levels in the hippocampus were also determined.n Results:The latency in the passive avoidance test in the model group was significantly shorter than that in the normal control group [(134.80 ± 33.89) s n vs. (282.20 ± 17.43) s, n t = 4.23, n P < 0.01]. The number of errors in the model group was significantly higher than that in the normal control group [(4.00 ± 1.58) n vs. (1.20 ± 1.30) times, n t = 2.85, n P < 0.01]. The latency in the passive avoidance test in the low-dose pine pollen (500 mg/kg) and high-dose pine pollen (1000 mg/kg) groups was significantly longer than that in the normal control group [(189.40 ± 27.21) s or (213.40 ± 21.26) s n vs. (134.80 ± 33.89) s, n t = 3.21, 4.38, all n P < 0.05]. The number of errors in the low-dose pine pollen (500 mg/kg) and high-dose pine pollen (1 000 mg/kg) groups was significantly lower than that in the normal control group [(1.60 ± 1.44) times or (1.40 ± 1.44) times n vs. (4.00 ± 1.58) times, n t = 5.12, 6.42, both n P < 0.05]. SOD activity and GSH, DA and NE levels in the hippocampus in the model group were significantly decreased compared with the normal control group [SOD: (7.59 ± 1.77) kU/g n vs. (39.90 ± 6.37) kU/g; GSH: (3.49 ± 0.13) mmol/g n vs. (6.37 ± 0.14) mmol/g; DA: (418.42 ± 2.57) ng/L n vs. (586.37 ± 3.64) ng/L; NE: (187.20 ± 5.41) ng/L n vs. (298.42 ± 2.32) ng/L, n t = 3.67, 8.23, 2.23, 3.65, all n P < 0.05]. MDA, IL-6 and TNF-α levels in the hippocampus in the normal control group were significantly higher than those in the model group [MDA: (8.79 ± 0.82) mmol/g n vs. (2.62 ± 0.16) mmol/g, IL-6: (48.07 ± 5.56) ng/L n vs. (18.76 ± 1.42) ng/L, TNF-α: (87.20 ± 4.31) ng/L n vs. (22.42 ± 3.39) ng/L, n t = 7.45, 2.67, 4.35, n P < 0.05 or n P < 0.01]. SOD activity, GSH, DA and NE levels in the hippocampus in the low-dose pine pollen (500 mg/kg) and high-dose pine pollen (1 000 mg/kg) groups were significantly higher than those in the model group [SOD: (18.80 ± 2.39) kU/g, (28.70 ± 2.36) kU/g n vs. (7.59 ± 1.77) kU/g, GSH: (5.04 ± 0.36) mmol/g, (5.45 ± 0.17) mmol/g n vs. (3.49 ± 0.13) mmol/g, DA: (488.37 ± 3.46) ng/L, (506.29 ± 5.72) ng/L n vs. (418.42 ± 2.57) ng/L, NE: (225.65 ± 3.72) ng/L, (239.76 ± 5.58) ng/L n vs. (187.20 ± 5.41) ng/L, n t = 4.56 or 6.71, n t = 4.65 or 5.32, n t = 4.73 or 6.72, n t = 3.84 or 5.63, n P < 0.05 or n P < 0.01]. MDA, IL-6 and TNF-α levels in the hippocampus in the low-dose pine pollen (500 mg/kg) and high-dose pine pollen (1 000 mg/kg) groups were significantly lower than those in the model group [MDA: (5.72 ± 0.47) mmol/g, (3.77 ± 0.23) mmol /g n vs. (8.79 ± 0.82) mmol/g, IL-6: (28.42 ± 3.54) ng/L, (23.43 ± 5.62) ng/L n vs. (48.07 ± 5.56) ng/L, TNF-α: (48.87 ± 4.82) ng/L, (39.65 ± 6.69) ng/L n vs. (87.20 ± 4.31) ng/L, n t = 6.31 or 7.28, n t = 3.46 or 6.31, n t = 4.28 or 3.57, n P < 0.05 or n P < 0.01].n Conclusion:Pine pollen can improve LPS-induced learning and memory impairments possibly through up-regulating the levels of monoamine neurotransmitters DA and NE and inhibiting the levels of oxidative stress and inflammatory reaction in the hippocampus of mice.