Figure 5.

T. gondii inhibited AgNP-induced mitochondrial apoptosis in ARPE-19 cells. ARPE-19 cells were pre-infected with T. gondii at MOI 5 for 2 h, and then treated with or without 5 μg/mL AgNPs for 24 h. (A,B,D) Pro-apoptosis (A,D) and pro-survival (B) Bcl-2 family protein levels were evaluated by Western blotting. (C) Mitochondrial and cytosolic fractions were analyzed for the expression of cytochrome c. COX IV and α-Tubulin were used as markers of mitochondria and cytosol, respectively. (E) JC-1 staining was observed by confocal imaging. In JC-1 stained cells, red fluorescence is visible in cells with high mitochondrial membrane potential, while green fluorescence of JC-1 monomer is present in cells with low mitochondrial potential. All data shown are representative of 3 independent experiments with similar results.

Abbreviations: AgNPs, silver nanoparticles; MOI, multiplicity of infection; Bcl-2, B-cell lymphoma 2; Bad, Bcl-2-associated death promoter; Bax, Bcl-2-associated X protein; Bik, BCL2-interacting killer; Bim, Bcl-2-like protein 11; Bid, BH3 interacting domain death agonist; Bak, BCL2-antagonist/killer; Puma, p53 upregulated modulator of apoptosis; Bcl-xL, B-cell lymphoma-extra large; Mcl-1, myeloid cell leukemia 1; COX, Cytochrome c oxidase; JC-1, 5.5′,6,6′-Tetrachloro-1,1′,3,3′-tetraethyl-imidacarbocyanine iodide; DAPI, 4ʹ,6-diamidino-2-phenylindole