Objective To investigate whether telomerase was involved in the neuroprotective effect of curcumin a-gainst Aβ. Methods Aβ1-42 (10μg/mL) was used to establish a damaged cell model and curcumin (10μg/mL) was used in treatment groups. Cell survival and cell growth,intracellular oxidative stress and hTERT expression was measured. After RNA interference,the effects of curcumin on cells were verified. Results Exposure to Aβ1-42 resulted in signifi-cant oxidative stress and cell toxicity,and the expression of hTERT was significantly decreased (P<0. 001). Curcumin pro-tected SK-N-SH cells from Aβ1-42 and up-regulated the expression of hTERT (P<0. 001). However,when telomerase ac-tivity was inhibited by TERT siRNA,the neuroprotection by curcumin was whittled (P>0. 05). Conclusion The neuro-protective effect of curcumin against Aβdepends on telomerase activity,and thus telomerase may be a target for therapeutic effect of curcumin.%目的：探讨端粒酶在姜黄素治疗β淀粉样蛋白(Aβ)损伤的神经保护效应中的作用。方法用Aβ1-42(10μg/mL)预处理SK-N-SH细胞建立损伤的细胞模型后,用姜黄素(10μg/mL)干预治疗组,处理前后检测细胞存活率、细胞内氧化应激水平及hTERT的表达水平,并通过RNA干扰技术降低hTERT的表达,以此验证端粒酶在姜黄素的干预作用中所起的作用。结果 Aβ1-42预处理组的氧化应激水平及细胞毒性均有显著增高( P<0.001),hTERT的表达水平明显下降(P<0.001)。姜黄素干预使SK-N-SH细胞免受Aβ1-42损伤(P<0.001)并上调hTERT的表达水平(P<0.001)。而当端粒酶活性被TERT的小分子干扰RNA抑制后,姜黄素的神经保护作用也随之消失(P>0.05)。结论姜黄素对抗Aβ毒性的神经保护作用有赖于端粒酶活性,端粒酶则可能是姜黄素治疗效应的靶点。
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