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Fig. 5 | Inflammation and Regeneration

Fig. 5

From: Targeting microglial autophagic degradation of the NLRP3 inflammasome for identification of thonningianin A in Alzheimer’s disease

Fig. 5

TA ameliorates neuronal damage induced by the Aβ(1–42)-induced activation of the NLRP3 inflammasome in microglial cells. BV-2 cells were treated with 5 μM of Aβ(1–42) for 24 h, followed by the treatment of TA (10 μM) in the presence or absence of inhibitors, including LY, CC, and SCH for an additional 24 h. The conditioned mediums were then transferred into PC-12 cells and incubated for 24 h. The cell viability of PC12 cells was then detected by (A) MTT assay, (B) Hoechst 33342/PI staining, and (C) flow cytometry methods. Bar charts indicate the cell viability, the PI/Hoechst ratio, and the apoptosis rate of PC-12 cells. The representative fluorescence images were captured by a fluorescence microscope. Magnification, × 20; scale bar: 100 μm. D Mouse primary microglial cells were treated with 5 μM of Aβ(1–42) for 24 h, followed by the treatment of TA at the indicated concentrations for 24 h. The conditioned mediums were then transferred into mouse primary hippocampal neurons and incubated for 24 h. The cell viability of mouse primary hippocampal neurons was then detected by Hoechst 33342/PI staining method. The representative fluorescence images were captured by a fluorescence microscope. Magnification, × 20; scale bar: 100 μm. The bar chart indicates the PI/Hoechst ratio of mouse primary hippocampal neurons. Error bars, S.D. *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001. n = 3. (One-way ANOVA with Tukey-corrected post hoc t-test for multiple comparisons was applied for comparison between groups)

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