N-乙酰-L-色氨酸减轻H2O2诱导小鼠海马神经元细胞凋亡

 目的 探讨N-乙酰-L-色氨酸(L-NAT)对海马神经元（PHN）缺血低氧损伤的影响。方法 用600μmol/L H2O2诱导PHN制备海马神经元细胞凋亡模型，采用免疫荧光染色检测caspase-3的表达，Rhodamine 123染色检测线粒体膜势能（ΔΨm）的改变，台盼蓝染色检测细胞存活率，比色法检测caspase-3、乳酸脱氢酶（LDH）的活性，Western blot检测caspase-3及凋亡诱导因子（AIF）和细胞色素C（CytC）等线粒体促凋亡因子在胞质蛋白和线粒体蛋白中的表达。结果 L-NAT可减轻H2O2所引起的细胞形态的死亡、存活率的降低、LDH的释放、caspase-3的激活、线粒体膜势能的丧失及AIF和CytC等线粒体促凋亡因子的释放。 结论 L-NAT能通过抑制caspase依赖性和非依赖性的细胞凋亡途径，减轻H2O2诱导的小鼠海马神经元的细胞损伤。

N-acetyl-L-tryptophan alleviates the apoptosis induced by H2O2 of mice PHNs

Objective To investigate the effects of N-acetyl-L-tryptophan (L-NAT) on H2O2-induced apoptosis of primary hippocampal neurons (PHN). Methods The apopotosis modle of PHN, a cellular model of cerebral ischemia, was made by H2O2. Immunofluorescence staining was used to detect the expression of caspase-3, Rhodamine 123 staining was used to detect mitochondrial membrane potential changes, trypan blue staining was used to detect survival rate, the colorimetric assay was used to detect the activity of caspase-3 and LDH, Western blot was used to detect the expressions of caspase-3 and apoptosis-inducing factor and cytochrome C and other mitochondrial pro-apoptotic factor in the cytosolic proteins and mitochondrial proteins. Results L-NAT inhibits H2O2-induced cell death, loss of mitochondrial membrane potential, downstream release of LDH and mitochondrial factors, and activation of caspase-3 in primary hippocampal neurons. Conclusions L-NAT had effectiveness on cerebral ischemia/hypoxia injury though caspase-independent and caspase-dependent apoptosis pathway.