CAJ | 학술논문

目的：观察调心方对由TNFα加Aβ(25～35)诱导的SK-N-SH(神经源性细胞株)细胞毒性的保护作用。方法：用TNFα 50ng/ml和Aβ(25～35)0.1μM处理SK-N-SH细胞造成细胞损伤模型。以MTT和DNA ladder为指标。结果：TNFα和Aβ(25～35)处理SK-N-SH细胞24小时细胞生存率减少约50%，而调心方含药血清能提高细胞模型的生存率，减少细胞DNA的降解。结论：一定剂量的TNFα加小剂量的Aβ(25～35)能造成接近体内病理生理机制的细胞损伤模型，调心方对TNFα加Aβ(25～35)造成的细胞毒性具有一定的保护作用。
목적：관찰조심방대유TNFα가Aβ(25～35)유도적SK-N-SH(신경원성세포주)세포독성적보호작용。방법：용TNFα 50ng/ml화Aβ(25～35)0.1μM처리SK-N-SH세포조성세포손상모형。이MTT화DNA ladder위지표。결과：TNFα화Aβ(25～35)처리SK-N-SH세포24소시세포생존솔감소약50%，이조심방함약혈청능제고세포모형적생존솔，감소세포DNA적강해。결론：일정제량적TNFα가소제량적Aβ(25～35)능조성접근체내병리생리궤제적세포손상모형，조심방대TNFα가Aβ(25～35)조성적세포독성구유일정적보호작용。
The effects of Heart Benefiting Receipt (HBR) on Aβ（25～35） plus TNFα induced toxicity was investigated in human neuroblastoma cell line SK-N-SH by measuring the mitochondria activity and DNA laddering. Treatment of SK-N-SH cells for 24 hours with TNFα 50ng/ml plus Aβ (25～35) 0.1μM resulted in a significant inhibition on MTT reduction (50%) when the normal control was defined as 100%. HBR was found in clinical relevant concentration to attenuate TNFα 50ng/ml plus Aβ (25～35) 0.1μM induced toxicity in SK-N-SH cells and DNA degradation. This study demonstrates that TNFα 50ng/ml plus Aβ (25～35) 0.1μM can mimic patho-physiological condition which might happen in patients with Alzheimer's disease, and HBR can exert neuroprotective properties which might be of importance and contribute to cliniccal efficacy to treatment of Alzheimer's Disease.