[Effects of moxa smoke through olfactory pathway on learning and memory ability in rapid aging mice].

To observe the effects of moxa smoke through olfactory pathway on learning and memory ability in rapid aging (SAMP8) mice, and to explore the action pathway of moxa smoke.Forty-eight six-month-old male SAMP8 mice were randomly divided into a model group, an olfactory dysfunction group, a moxa smoke group and an olfactory dysfunction + moxa smoke group, with 12 mice in each group. Twelve age-matched male SAMR1 mice were used as the blank group. The olfactory dysfunction model was induced in the olfactory dysfunction group and the olfactory dysfunction + moxa smoke group by intraperitoneal injection of 3-methylindole (3-MI) with 300 mg/kg, and the moxa smoke group and the olfactory dysfunction + moxa smoke group were intervened with moxa smoke at a concentration of 10-15 mg/m3 for 30 min per day, with a total of 6 interventions per week. After 6 weeks, the emotion and cognitive function of mice was tested by open field test and Morris water maze test, and the neuronal morphology in the CAI area of the hippocampus was observed by HE staining. The contents of neurotransmitters (glutamic acid [Glu], gamma-aminobutyric acid [GABA], dopamine [DA], and 5-hydroxytryptamine [5-HT]) in hippocampal tissue of mice were detected by ELISA.The mice in the blank group, the model group and the moxa smoke group could find the buried food pellets within 300 s, while the mice in the olfactory dysfunction group and the olfactory dysfunction + moxa smoke group took more than 300 s to find them. Compared with the blank group, the model group had increased vertical and horizontal movements (P<0.05) and reduced central area residence time (P<0.05) in the open field test, prolonged mean escape latency on days 1-4 (P<0.05), and decreased search time, swimming distance and swimming distance ratio in the target quadrant of the Morris water maze test, and decreased GABA, DA and 5-HT contents (P<0.05, P<0.01) and increased Glu content (P<0.05) in hippocampal tissue. Compared with the model group, the olfactory dysfunction group had increased vertical movements (P<0.05), reduced central area residence time (P<0.05), and increased DA content in hippocampal tissue (P<0.05); the olfactory dysfunction + moxa smoke group had shortened mean escape latency on days 3 and 4 of the Morris water maze test (P<0.05) and increased DA content in hippocampal tissue (P<0.05); the moxa smoke group had prolonged search time in the target quadrant (P<0.05) and increased swimming distance ratio, and increased DA and 5-HT contents in hippocampal tissue (P<0.05, P<0.01) and decreased Glu content in hippocampal tissue (P<0.05). Compared with the olfactory dysfunction group, the olfactory dysfunction + moxa smoke group showed a shortened mean escape latency on day 4 of the Morris water maze test (P<0.05). Compared with the moxa smoke group, the olfactory dysfunction + moxa smoke group had a decreased 5-HT content in the hippocampus (P<0.05). Compared with the blank group, the model group showed a reduced number of neurons in the CA1 area of the hippocampus with a disordered arrangement; the olfactory dysfunction group had similar neuronal morphology in the CA1 area of the hippocampus to the model group. Compared with the model group, the moxa smoke group had an increased number of neurons in the CA1 area of the hippocampus that were more densely packed. Compared with the moxa smoke group, the olfactory dysfunction + moxa smoke group had a reduced number of neurons in the CA1 area of the hippocampus, with the extent between that of the moxa smoke group and the olfactory dysfunction group.The moxa smoke could regulate the contents of neurotransmitters Glu, DA and 5-HT in hippocampal tissue through olfactory pathway to improve the learning and memory ability of SAMP8 mice, and the olfactory is not the only effective pathway.目的：观察艾烟干预经嗅觉途径对快速老化（SAMP8）小鼠学习记忆的影响，探究艾烟的作用途径。方法：将48只6月龄雄性SAMP8小鼠随机分为模型组、嗅觉障碍组、艾烟组、嗅觉障碍+艾烟组，每组12只；以12只同月龄雄性正常老化（SAMR1）小鼠作为空白组。嗅觉障碍组和嗅觉障碍+艾烟组以300 mg/kg 3-甲基吲哚（3-MI）腹腔注射制备嗅觉障碍模型，艾烟组和嗅觉障碍+艾烟组每日以10~15 mg/m3浓度艾烟干预30 min，每周干预6 d。6周后进行旷场实验、Morris水迷宫实验检测小鼠的情绪和学习记忆能力，HE染色观察海马CAI区神经元形态，ELISA法检测小鼠海马组织神经递质[谷氨酸（Glu）、γ-氨基丁酸（GABA）、多巴胺（DA）、5-羟色胺（5-HT）]含量。结果：空白组、模型组和艾烟组小鼠均可在300 s内寻找到埋藏的食物小球；嗅觉障碍组和嗅觉障碍+艾烟组小鼠找寻时间均>300 s，提示嗅觉障碍模型制备成功。与空白组比较，模型组小鼠旷场实验垂直运动次数、水平运动次数增加（P<0.05），中央区停留时间缩短（P<0.05），Morris水迷宫实验第1~4天平均逃避潜伏期延长（P<0.05），目标象限搜索时间、目标象限游程、目标象限游程比及海马组织GABA、DA、5-HT含量均降低（P<0.05，P<0.01），海马组织Glu含量升高（P<0.05）。与模型组比较，嗅觉障碍组小鼠垂直运动次数增加（P<0.05），中央区停留时间缩短（P<0.05），海马组织DA含量升高（P<0.05）；嗅觉障碍+艾烟组第3、4天平均逃避潜伏期缩短（P<0.05），海马组织DA含量升高（P<0.05）；艾烟组小鼠目标象限搜索时间延长（P<0.05），目标象限游程比及海马组织DA、5-HT含量均升高（P<0.05，P<0.01），海马组织Glu含量降低（P<0.05）。与嗅觉障碍组比较，嗅觉障碍+艾烟组第4天平均逃避潜伏期缩短（P<0.05）。与艾烟组比较，嗅觉障碍+艾烟组小鼠海马组织5-HT含量降低（P<0.05）。与空白组比较，模型组小鼠海马CA1区神经元数量减少，排列疏松紊乱；嗅觉障碍组小鼠海马CA1区神经元细胞形态与模型组相似；与模型组比较，艾烟组小鼠海马CA1区神经元数量增多且更加密集；与艾烟组比较，嗅觉障碍+艾烟组小鼠海马组织CA1区神经元细胞数量减少，程度介于艾烟组与嗅觉障碍组之间。结论：艾烟可能通过嗅觉调节海马组织神经递质Glu、DA、5-HT含量，改善SAMP8小鼠的学习记忆能力，且嗅觉并非艾烟起效的唯一途径。.