中文摘要：

目的：通过建立星形胶质细胞氨中毒的模型，探讨瞬时受体电位M2（TRPM2）阳离子通道在其中发挥的作用。方法：分离并培养小鼠原代星形胶质细胞。实验分为5组：对照组、氯化铵处理组、氯化铵＋3-氨基苯甲酰胺（3-AB）处理组、氯化铵＋PJ-34处理组和TRPM2基因敲除小鼠＋氧化铵处理组。测定细胞的活性、caspase-3活性、细胞坏死和体积大小，以此来衡量氨中毒的程度。用全细胞膜片钳记录TRPM2通道电流变化。结果：氯化铵引起细胞肿胀伴随着细胞坏死。聚腺苷二磷酸核糖聚合酶（PARP）抑制剂3-AB和PJ-34抑制了氯化铵引起的阳离子电流，并减轻了氯化铵引起的相应细胞伤害。TRPM2基因敲除小鼠组细胞的伤害明显减轻（P〈0．01）。结论：TRMP2通道的激活是细胞暴露于氯化铵后发生肿胀、坏死的必要步骤；氯化铵诱导的星形胶质细胞肿胀与坏死密切相关。

英文摘要：

AIM： To study the effects of transient receptor potential melastatin 2 （TRPM2） cation channel on ammonia intoxication in astrocytes. METHODS： Primary astrocytes were isolated, cultured and divided into 5 groups： control group, ammonium chloride （ NH4 CI ） treatment group ; NH4 C1 ＋ 3-aminobenzamide （ 3-AB ） treatment group, NH4C1 ＋P J-34 treatment group, and TRPM2 knockout ＋ NH4CI treatment group. Cell viability, caspase-3 activity, cell necrosis and cell volume were measured to assess the extent of ammonia toxicity. Whole-cell patch-clamp was performed to record the currents via TRPM2 channels. RESULTS： NI-I4 C1 caused cell swelling accompanied with cell necrosis. The 13o- ly（ADP-ribose） polymerase （PARP） inhibitors, 3-AB and PJ-34, inhibited the cation currents activated by NH4 C1, and attenuated NH4Cl-induced cell damage. In TRPM2-deficient astrocytes, decreased cell damage was observed. CONCLU- SION： TRPM2 activation is essential for cell swelling and necrosis in astrocytes exposed to NH4 C1. NH4 Cl-triggered astro- cyte swelling is closely correlated with necrosis.