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. 2022 Nov 18;11(22):3665. doi: 10.3390/cells11223665

Figure 3.

Figure 3

NPY treatment suppresses the activation of pro-apoptotic JNK induced by glutamate in SH-SY5Y cell cultures. Western blot analysis illustrates the glutamate induced phosphorylation of JNK (T183/Y185), while NPY treatments (glutamate + NPY) reduced the phosphorylation of JNK at 12 h (A) and densitometric quantification of JNK2 (B) and JNK1 (C) phosphorylation indicates a significant increase in phosphorylation of JNK induced by glutamate compared to control (F(1,16)= 102 in Figure (B) and F(1,16)= 67.85 in Figure (C), **** p < 0.0001, n = 3) and a concentration-dependent decrease with NPY treatments at 12 h (F(3,16) = 34.88 in Figure (B) and F(3,16) = 25.90 in Figure (C), **** p  <  0.0001 represents significance between glutamate and glutamate + NPY group (red), n = 3). Western immunoblot analysis for 24 h treatment (D) and their densitometric quantification of JNK2 (E) and JNK1 (F) phosphorylation levels indicates a significant increase in phosphorylation of JNK induced by glutamate compared to control (F(1,16)= 59.13 in Figure (E) and F(1,16)= 64.77 in Figure (F), **** p  <  0.0001, n = 3) and a concentration dependent decrease with NPY treatments (F(3,16) = 7.82 in Figure (E) and F(3,16) = 7.926 in Figure (F), *** p  <  0.001 and **** p  <  0.0001 represents significance between glutamate and glutamate + NPY group (purple), n = 3). (G) Immunofluorescence images (representative) of treated SH-SY5Y cells showing the expression of phosphorylated JNKs. After 12 h of treatment, cells were fixed and immunostained with an anti-phospho-JNK (T183/Y185) antibody (red). Nuclei were stained with DAPI (blue). Scale bar = 10 μm.