香烟烟雾与慢性应激联合暴露对大鼠学习记忆能力的影响

目的：研究香烟烟雾与慢性应激联合暴露对大鼠学习记忆能力的影响。方法：40只SPF级SD大鼠，每组10只，雌雄各半，随机分为对照组、香烟烟雾组、慢性应激组、联合干预组。对照组不采取任何处理；香烟烟雾组大鼠采用呼吸道静式染毒，每天1次，每次10支香烟，每次1 h，连续12周；慢性应激组从5种慢性应激方案中每日随机给予1种慢性应激，每种慢性应激方式不连续应用，进行12周；联合干预组每日进行慢性应激处理的同时吸烟10支，持续12周。在染毒第2、4、8、10、12周时，各组大鼠进行Morris水迷宫实验，检测大鼠逃避潜伏期，测试各组大鼠学习记忆能力。染毒12周后，腹主动脉采血，剥取大脑，观察大鼠体质量、脑质量、脑脏器系数、脑组织病理学变化，测定血清中Cort浓度、ACH、CHAT含量及ACHE活力。结果：与对照组比较，慢性应激组大鼠Cort浓度显著增加（P < 0.05），提示慢性应激组大鼠处于紧张状态；与慢性应激组比较，第2周联合干预组逃避潜伏期潜伏期减少，呈拮抗作用（P < 0.05）；与对照组比较，香烟烟雾、慢性应激单独及联合干预组大鼠第10周逃避潜伏期增加（P < 0.05）；病理学观察结果显示香烟烟雾组大鼠神经元轻度核固缩，脑膜血管中度充血及轻度出血，胶质细胞增生，慢性应激组大鼠神经元可见轻度核固缩及淤血，联合干预组变化最明显，联合干预组大鼠神经元中度核固缩，脑膜轻度淤血及水肿，神经元周围空泡形成。与对照组比较，二者单独及联合暴露组大鼠ACH含量下降（P < 0.05），与对照组比较，应激组大鼠CHAT含量下降、ACHE活力升高（P < 0.05）。结论：香烟烟雾和慢性应激联合暴露对大鼠学习记忆能力的影响存在交互作用；香烟烟雾和慢性应激单独及联合暴露均会导致大鼠学习和记忆能力下降；二者单独及联合暴露主要通过造成ACH合成受损，导致大鼠学习和记忆能力降低；联合暴露对ACH、CHAT含量及ACHE活力未产生交互作用；其联合作用具体机制需进一步深入研究。

Combined effects of cigarette smoke and chronic stress on learning and memory in rats

OBJECTIVE: To study the effects of cigarette smoke exposure and chronic stress on learning and memory in rats. METHODS: 40 SPF SD rats,10 in each group,50% males,were randomly divided into non-exposed control,cigarette smoke,chronic stress and the combined groups. Rats in the cigarette smoke group were exposed to the virus by respiratory statics,once a day,10 cigarettes each time for 1 h,for 12 weeks. In the chronic stress group,one chronic stress was randomly given every day from five chronic stress programs,and each chronic stress mode was applied discontinuously for 12 weeks. The combined group was treated with chronic stress and smoked 10 cigarettes a day,for 12 weeks. In the 2,4,8,10,12 weeks,the Morris water maze experiment in rats was conducted,constituting the escape latency of rats,test of 4 group rats' learning and memory ability,infected after 12 weeks,abdominal aortic blood,wring the brain,rat body mass,brain,brain viscera coefficient,brain tissue pathology changes,and determination of Cort concentrations,ACH,CHAT content and ACHE activity in serum. RESULTS: Compared with the control group,Cort concentrations in the chronic stress group was significantly increased (P < 0.05),indicating that the rats in the chronic stress group were under stress. Compared with the chronic stress group,the latency of escape at week 2 in the combined group was decreased and showed an antagonistic effect (P < 0.05). Compared with the control group,the latencies of escape at week 10 in the three treated groups were increased (P < 0.05). Pathology results from the cigarette smoke group show rat neurons mild nuclear pyknosis,meningeal vascular moderate hyperemia and mild bleeding,glial cell hyperplasia,chronic stress group rats neurons,visible light nuclear pyknosis and congested,joint intervention group change is most obvious,joint intervention group rat neurons moderate nucleus pyknosis,meningeal congestion and edema of the mild,neurons around the cavity formation. Compared with the control group,the ACH content of rats in the three treated groups were decreased (P < 0.05),while the CHAT content of rats in the stress group decreased and ACHE activity increased (P < 0.05). CONCLUSION: The effects of combined cigarette smoke and chronic stress were interactive on the learning and memory ability of rats. In addition,learning and memory in rats were reduced in the three treated groups. Furthermore,the synthesis of ACH was impaired which was associated with reduced learning and memory ability of rats. The combined exposure did not interact with ACH,CHAT content and ACHE activity. The specific mechanism of its joint action needs to be further studied.