Figure 2 | Scientific Reports

Figure 2

From: Cilostazol restores autophagy flux in bafilomycin A1-treated, cultured cortical astrocytes through lysosomal reacidification: roles of PKA, zinc and metallothionein 3

Figure 2The alternative text for this image may have been generated using AI.

PKA may mediate the effects of cilostazol and cAMP. (a) Cilostazol and cAMP activate PKA in astrocytes. Western blot analysis of p-PKA in cells treated with 10 μM cilostazol (+Cilo) or 300 μM cAMP alone (+cAMP), or together with 10 μM H-89 (+PKAi), a PKA inhibitor, for 1 hour. H-89 reversed cilostazol- or cAMP-induced increases in p-PKA levels. Bars denote the ratio of p-PKA bands to corresponding total PKA bands. Data are presented as means ± SEM (n = 7; * denote P < 0.05, ** denote P < 0.01 compared with CTL, Cilo, cAMP or PKAi, Two-tailed Student’s t-test for 2 comparisons). (b) DND-189 fluorescence in astrocytes before (CTL) and after a 60-minute exposure to BafA1 (BA), BafA1 plus cilostazol (BA + Cilo), BafA1 plus cAMP (BA + cAMP) or BafA1 plus forskolin (BA + forsk), in the absence or presence of PKAi (BA + PKAi) (Scale bar, 20 μm). (c) Bars indicate relative changes in the fluorescence intensity. Values for individual bars were normalized to control values (mean ± SEM; n = 4; * denote P < 0.05 compared with BA, Cilo, cAMP, forsk or PKAi; Two-tailed Student’s t-test for 2 comparisons).

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