Skip to main content
. 2022 Nov 18;11(22):3665. doi: 10.3390/cells11223665

Figure 4.

Figure 4

NPY treatment inhibits pro-apoptotic BAD phosphorylation caused by glutamate in SH-SY5Y cell cultures. Western immunoblot analysis for phosphorylation of BAD at Ser 128 under glutamate and NPY treatments (glutamate + NPY) at 12 h (A) and the densitometric quantification of phospho-BAD (B) reveals a significant increase in BAD activation under glutamate stress compared to control (F(1,16) = 108.1, **** p  <  0.0001, n = 3) and a decrease with NPY treatment at 12 h (F(3,16) = 7.4, **** p  < 0.0001 represents significance between glutamate and glutamate + NPY (red), n = 3). Western immunoblot analysis for 24 h treatment (C) and the densitometric quantification of phospho-BAD (D) reveals a significant increase in BAD activation under glutamate stress compared to control (F(1,16) = 116.1, **** p  <  0.0001, n = 3), and a decrease with NPY treatments at 24 h (F(3,16) = 7.594, ** p  <  0.01 and **** p  <  0.0001 represents significance between glutamate and glutamate + NPY (purple), n = 3). Each band intensity was normalized to the respective band intensity of β-actin. (E) Immunofluorescence images (representative) of treated SH-SY5Y cells showing the expression of phosphorylated Bad. After 12 h of treatment, cells were fixed and immunostained with an anti-phospho-Bad (Ser 128) antibody (red). Nuclei were stained with DAPI (blue). Scale bar = 10 μm.