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目的:在成功建立目前公认的老年性痴呆(AD)体外模型基础上,观察补肾化痰益智法抗炎治疗AD的作用及机制。方法:运用Aβ1-42作用于BV-2细胞,同时用补肾化痰益智方含药血清进行干预,以吲哚美辛为对照。ELISA法检测细胞释放白介素-1β(IL-1β)、白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)的情况,RT-PCR法检测IL-1βmRNA的表达。结果:补肾化痰益智组与吲哚美辛组比较,能够更有效抑制IL-1β的表达(P<0.05),并能够从基因水平调节IL-1βmRNA的表达,从而抑制BV-2细胞分泌炎性因子的作用。结论:Aβ神经毒性与AD免疫炎性反应具有相关性。补肾化痰益智法能够调控炎性细胞因子IL-1β、IL-6、TNF-α及IL-1βmRNA的表达,从基因水平抑制炎性反应。
OBJECTIVE: To observe the effect and mechanism of Kidney-Nourishing, Phlegm-Resolving, and Nervous System anti-inflammatory therapy on AD based on the successful establishment of the currently accepted model of Alzheimer’s disease (AD) in vitro. Methods: The effect of Aβ1-42 on BV-2 cells was observed with the intervention of Bushen Huatan Yizhi Decoction-containing serum. Indomethacin was used as control. The levels of IL-1β, IL-6 and TNF-α were detected by ELISA. The expression of IL-1βmRNA was detected by RT-PCR. Results: Compared with indometacin group, Bushen Huatan Yizhi could inhibit the expression of IL-1β more effectively (P <0.05) and regulate the expression of IL-1β mRNA at the gene level, thereby inhibiting the secretion of BV-2 cells The role of inflammatory factors. Conclusion: The neurotoxicity of Aβ is correlated with AD immune-inflammatory reaction. Bushen Huatan Yizhi Act can regulate the expression of inflammatory cytokines IL-1β, IL-6, TNF-α and IL-1βmRNA, and inhibit inflammatory reaction at gene level.