目的：探讨苯并［a］芘［benzo(a)pyrene，BaP］对神经胶质细胞中具有β-淀粉体（β-amyloid，Aβ）清除作用的胰岛素降解酶（insulin-degrading enzyme，IDE）及脑啡肽酶（neprilysin，NEP）表达的影响。方法：制备新生SD大鼠原代神经胶质细胞混合培养体系，接受不同浓度的BaP、Aβ1-42寡聚体、Aβ1-42纤维体单独或联合处理24 h后，采用细胞增殖毒性检测试剂盒测定细胞存活率。随机分为对照组、BaP（2.00 μmol/L）组、Aβ1-42（20.00 mg/L）寡聚体组、BaP+Aβ1-42寡聚体组、Aβ1-42（20.00 mg/L）纤维体组、BaP+Aβ1-42纤维体组，其中BaP均为预处理12 h后再与不同聚集状态的Aβ1-42共同作用。进一步采用实时荧光定量PCR及蛋白质免疫印迹技术检测体系中IDE、NEP的mRNA和蛋白表达水平。结果：20.00 μmol/L及以下浓度的BaP处理，20.00、40.00 mg/L的Aβ1-42寡聚体或Aβ1-42纤维体单独处理，BaP与Aβ1-42寡聚体或BaP与Aβ1-42纤维体联合处理对神经胶质细胞的存活率均无明显影响。与对照组相比，BaP单独处理组中IDE、NEP的mRNA和蛋白水平均未明显改变；而Aβ1-42寡聚体单独作用可明显上调IDE的mRNA及蛋白水平（P<0.05），同时BaP预处理可显著抑制Aβ1-42寡聚体作用引起的IDE表达水平上调（P<0.05）；另一方面,Aβ1-42纤维体在单独处理或有BaP预处理情况下，IDE、NEP的mRNA和蛋白水平均未发生明显改变。结论：在对细胞存活率无明显影响的前提下，BaP预处理显著抑制了Aβ寡聚体作用后的IDE表达水平上调，提示苯并［a］芘可能干扰Aβ寡聚体降解途径导致Aβ增多聚集，进而可能促进认知功能降低及阿尔兹海默病的形成。

Objective： To investigate effects of benzo(a)pyrene (BaP) on expressions of insulin-degrading enzyme (IDE) and neprilysin (NEP) which have the ability to degrade β-amyloid (Aβ) in neu-roglia cells. Methods: Primary mix-neuroglia cells were cultured from newborn SD rats. After exposure to BaP, Aβ1-42 oligomer or Aβ1-42 fiber individually or jointly for 24 h, the cell survival rate was mea-sured by cell counting kit-8 (CCK-8). Afterwards, the primary mix-neuroglia cells were divided randomly into six groups: Control group, BaP group (2.00 μmol/L), Aβ1-42 oligomer group (20.00 mg/L), BaP plus Aβ1-42 oligomer group, Aβ1-42 fiber group (20.00 mg/L) and BaP plus Aβ1-42 fiber group, of which BaP was pretreated for 12 h followed by cotreatment with different aggregated Aβ1-42. The expressions of IDE and NEP were measured by quantitative real-time polymerase chain reaction (qRT-PCR) for mRNA level and Western blotting for protein level. Results： The cell survival rate showed no significant differences after treatment with BaP (≤20.00 μmol/L), Aβ1-42 oligomer (20.00, 40.00 mg/L), Aβ1-42 fiber (20.00, 40.00 mg/L) or cotreatment with BaP and Aβ1-42 oligomer or BaP and Aβ1-42 fiber. Compared with the control group, expressions of IDE and NEP in BaPtreated alone group had no obvious change; however, exposure to Aβ1-42 oligomer alone significantly increased the mRNA and protein level of IDE (P<0.05), and the BaP pretreatment could significantly inhibit the up-regulated expressions of IDE by Aβ1-42 oligomer (P<0.05); on the other hand, exposure either to Aβ1-42 fiber alone or under the BaP pretreatment did not change the mRNA and protein level of IDE and NEP obviously. Conclusion: On the premise of no significant change of cell survival rate, BaP pretreatment inhibited the up-regulated expressions of IDE in primary mixed neuroglia cells under cotreatment with Aβ oligomer, indicating that BaP may disturb degradation of Aβ oligomer and cause deposition of β-amyloid and further induce cognitive decline and acceleration of Alzheimer.