木犀草苷对阿尔茨海默病模型细胞凋亡和炎性因子 表达的研究.

Objective To explore the effect and possible mechanism of cynaroside on apoptosis and expression of inflammatory factor in model cells of Alzheimer's disease (AD) by down-regulating mitogen-activated protein kinase kinase kinase 3 (MEKK3). Methods PC12 cells were cultured in vitro and incubated with different doses (6.25 mg/L, 12.5 mg/L, 25 mg/L) of cynaroside for 24 h to establish an AD cell model induced by Aβ25-35. In addition, MEKK3 small interfering RNA or overexpression vector was transfected into PC12 cells, and Aβ25-35 induced AD cell model was established after incubation with 25 mg/L luteolin for 24 h. CCK-8 was used to detect inhibition rate of cell proliferation, and flow cytometry was used to detect apoptosis rate. ELISA was used to detect inflammatory factors (TNF- α, IL-6, IL-1β). The protein expression of MEKK3 was detected by Western blot assay. Results Cynaroside could decrease the proliferation inhibition rate, apoptosis rate, inflammatory cytokines (TNF-α, IL-6, IL-1β) and MEKK3 protein expression in PC12 cells induced by Aβ25-35 (P＜ 0.05). Knockdown of MEKK3 could reduce the proliferation inhibition rate, apoptosis rate and inflammatory cytokines (TNFα, IL-6, IL-1β) of Aβ25-35-induced PC12 cells, while overexpression of MEKK3 showed the opposite effect. Upregulation of MEKK3 expression attenuated effects of cynaroside on the proliferation inhibition rate, apoptosis rate and inflammatory factors of Aβ25-35-induced PC12 cells. Conclusion Cynaroside may inhibit apoptosis and expression of inflammatory factors of AD model cells by down-regulating MEKK3, which has potential value in the treatment of AD. [ABSTRACT FROM AUTHOR]