【摘要】 目的 :观察调心方对由LPS诱导的PC12细胞毒性和Aβ生成的改善作用。 方法 :用LPS处理PC12细胞 (神经源性细胞株 )造成细胞损伤和Aβ生成增加的模型。以MTT测定和逆转录 聚合酶链反应、蛋白免疫印迹法及免疫细胞化学方法观察细胞的生存率和APP、CPP3 2的表达及细胞内Aβ生成的变化。 结果 :LPS处理PC12细胞 ,细胞生存率下降约 2 5 % ,APP、CPP3 2的表达和细胞内Aβ生成增加 ,而调心方的含药血清能提高细胞模型的生存率 ,降低APP、CPP3 2的表达和细胞内Aβ生成。 结论 :一定剂量的LPS能造成理想的细胞损伤和Aβ生成增加的模型 ,其机制可能与CPP3 2的双重作用有关 ,即参与APP的水解 ,造成Aβ生成增加和引起细胞的死亡或凋亡。调心方对LPS造成的细胞毒性具有一定的保护作用 ,并减少Aβ生成。更多还原

【Abstract】 The effects of Heart Benefiting Receipt (HB R) on LPS induced toxicity and Aβ formation was investigated in PC12 cell line. Methods: PC12 cells treated with LPS and LPS plu s HBR. Cell survival rate measured by MTT assay; Incellular Aβ production were assessed after treatment by immunocytochemistry assay; APP mRNA were detected by RT PCR; CPP32 expression were assessed by Western Blot an alysis at different time points (8h, 16h) after treatment. Results: Treatment of PC12 cells with LPS result ed in a significant inhibition of MTT reduction (25%) when the normal control wa s defined as 100% and APP mRNA transcription, CPP32 expression and Aβ formation increased. HBR was found in clinical relevant concentration to attenuate LPS induced toxicity in PC12 cells and reduce APP mRNA transcripti on, CPP32 expression and Aβ formation. Conclution: This study demonstrates that LPS can mimic patho physiological condition which might happen in patients with Alzhei mer’s disease. The effects of LPS may involves CPP32 which play a dual role in p roteolytic processing of APP and the resulting propensity for Aβ formation and in the ultimate cell death. HBR can exert neuroprotective p roperties which might be of importance and contribute to clinical efficacy to t reatment of Alzheimer’s Disease.更多还原