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. 2020 Apr 30;14:88. doi: 10.3389/fncel.2020.00088

FIGURE 1.

FIGURE 1

DOR inhibition or MOR activation aggravated Aβ1–42 oligomer induced cell injury. The experiments were conducted on highly differentiated PC12 cells (N = 3 in each group). The cell viability were measured every 24 h using CCK8 kit. C: normal control. A: Aβ1–42 oligomer (20 μM) to mimic AD cell injury (Aβ1–42 injury or AD injury). A + U: DOR activation with UFP-512 in AD injury. A + U + N: A + U plus DOR inhibition with naltrindole. A + N: DOR inhibition with naltrindole in AD injury. A + D: DADLE (1 μM) treatment in AD injury. A + M: MOR activation with 1 μM DAMGO in AD injury. (A) DOR/MOR induced morphologic changes in PC12 cells. Note that Aβ1–42 oligomer induced cell injury and the administration of DOR antagonist naltrindole or MOR agonist DAMGO aggravated such injury. Morphologically, it was characterized by a reduction in cell density, decrease of synapses. Scale bar = 100 μm in panel (A) for all groups. (B) Cell viability and DOR-mediated alternations in cell proliferation under AD injury. *p < 0.05, **p<0.01 vs. (C); Δ p<0.05, Δ Δ p < 0.01 vs. (A). Note that Aβ1–42 oligomer administration largely decreased the cell viability, and DOR inhibition further aggravated the cell injury. (C) Effects of DADLE and DAMGO on cell viability in Aβ1–42 injury. *p < 0.05, **p<0.01 vs. (C); Δ Δ p < 0.01 vs. (A). Note that MOR activation greatly aggravated the cell viability at 72 h after Aβ1–42 oligomer administration.