Figure 3.

Effect of MKP1 on Aβ₄₂-induced neuroinflammation in PC12 cell culture.

(A) PC12 cells were treated without (Control) or with 10 μM Aβ₄₂ (Aβ₄₂), and PC12 cells stably expressing MKP1 shRNA (Aβ₄₂ + MKP1 KD) or MKP1 lentiviral particles (Aβ₄₂ + MKP1) were treated with 10 μM Aβ₄₂ for 24 hours. Total protein was extracted for western blot assay for p-JNK with GAPDH as loading control. The relative expression of p-JNK to GAPDH was assessed by densitometric analysis using ImageJ software. (B) Cells were treated as in A. Total RNA was extracted for quantitative real time-polymerase chain reaction for TNF-α and IL-1β mRNA with GAPDH as internal control. Data are representative images or are expressed as the mean ± SD (six separate experiments for each group of cells). Intergroup comparison was performed with analysis of variance. #P < 0.05, vs. Aβ₄₂ group. MKP1: Mitogen-activated protein kinase phosphatase 1; Aβ₄₂: amyloid beta 42; p-JNK: phospho-c-Jun N-terminal kinase; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; TNF-α: tumor necrosis factor-alpha; IL-1β: interleukin-1 beta.