丙烯酰胺亚急性中毒对大鼠神经元NOS表达的影响

Effect of acrylamide-induced subacute poisoning on the expression of NOS in rat neurons

【目的】观察丙烯酰胺(acrylamide,ACR)亚急性中毒大鼠海马各亚区及大脑皮质神经元形态改变及一氧化氮合酶(nitric oxide synthase,NOS)的表达情况,探讨一氧化氮(nitric oxide,NO)在ACR神经中毒机制中的作用。【方法】随机将雄性SD大鼠20只分为对照组和ACR组。ACR组以50μg·(kg·d)-1的剂量腹腔注射ACR连续9 d以建立ACR亚急性中毒模型,对照组给予等量生理盐水。分别取海马和皮质组织进行尼氏染色观察神经变性,以烟酰胺腺嘌呤二核苷酸-黄递酶(nicotinamide adenine dinucleotide phosphate-diaphorase,NADPH-d)组织化学染色观察NOS的表达情况。【结果】尼氏染色显示ACR组大鼠海马CA1区神经元(P<0.001)和皮质区神经元数目(P<0.05)明显减少,而CA3区和齿状回区神经元数目无明显变化(P>0.05)。NADPH-d染色显示ACR组NOS阳性神经元数目在海马各区及大脑皮质均较对照组明显增多,且NOS阳性神经元染色较深(呈紫蓝或深蓝色)。【结论】ACR亚急性中毒时NO可能介导了神经元的损伤过程。

A total of 20 male SD rats were randomly divided into control group and ACR group. Rat models with ACR-indueed suhaeute poisoning model were established with the daily intraperitoneal injection of ACR in a dose of 50 μg· （ kg·d）^-1 for 9 consecutive days. Rats in the control group were given equal amount of normal saline. Nissl staining and NADPH-d histochemieal staining were carried out in the hippoeampus and cortex tissues to observe the neural degeneration and the expression of NOS respectively. [ Results] Nissl staining showed that the number of neurons in the ACR group decreased obviously in CA1 area （P 〈 0.001） and cortex （P 〈 0.05）, while there was no significant change in CA3 area and dentate gyms （P 〉 0.05）. NADPH-d staining showed that the number of NOS positive neurons in the hippocampus and cerebral cortex of the ACR group was much more than that of the control group. Furthermore, NOS positive neurons were dyed deep （dark purple blue or dark blue）. [Conclusion] NO may mediate the damage process of neurons in ACR-induced subaeute poisoning.