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. 2019 Mar 4;13:61. doi: 10.3389/fncel.2019.00061

Figure 1.

Figure 1

Santacruzamate A (STA) attenuated amyloid-β protein fragment 25–35 (Aβ 25–35)-induced apoptosis and reversed Aβ25–35-induced unfolded protein response (UPR) and endoplasmic reticulum (ER) stress. (A) Effects of STA alone on the cell viability of PC12 cells. (B) Effects of STA alone on the cell viability of SH-SY5Y cells. (C) Protective effects of STA pretreatment on the Aβ 25–35-induced toxicity in PC12 cells. (D) Protective effects of STA pretreatment on the Aβ 25–35-induced toxicity in SH-SY5Y cells. (E) Effects of STA on lactate dehydrogenase (LDH) leakage in PC12 cells. (F) Effects of STA on caspase-3 activity in PC12 cells. (G) Effects of STA on the cell apoptosis rate in PC12 cells. Cell apoptosis was determined by annexin V/propidium iodide (PI) double staining kits using flow cytometry and quantification of the apoptosis rate. (H) TUNEL staining in PC12 cells. Representative images of TUNEL-positive cells (green, top row) and Hoechst counterstaining (blue, middle row) are shown, along with a histogram quantifying the TUNEL staining. Scale bar: 200 μm. This histogram shows the relative proportion of TUNEL-positive cells in different treatment groups. Cells were pre-incubated for 4 h with STA and then co-treated with Aβ 25–35 for 24 h. The untreated control group was incubated with the appropriate amount of vehicle. The results are expressed as the mean ± the standard deviation of three independent experiments. ##P < 0.01 vs. the control, *P < 0.05 vs. Aβ25–35 treatment, **P < 0.01 vs. Aβ25–35 treatment.