Fig 1: T. denticola and Aß1–42 induced apoptosis in N2a cells via a similar mechanism. (A) N2a cells were co-cultured with T. denticola, Aß1–40, and Aß1–42, and the apoptosis rate was examined using TUNEL staining. (B) The protein levels of cleaved caspase-3 in N2a cells in each group were examined by western blotting, and the results were quantitatively analyzed. (C) The protein levels of SAPK/JNK, BCL-W, and SMAC in N2a cells in each group were examined by western blotting, and the results were quantitatively analyzed. Results are presented as the mean ± SD, *: p < 0.05, ***: p < 0.001, n = 3 per experiment.
Fig 2: T. denticola oral infection regulated the expression levels of apoptosis-associated genes and proteins. (A) The gene expression levels of Bclw, Bcl2, Bik, Bax, Bak, Bad, Jnk2, Jnk3, and Smac in the hippocampi of mice were measured using Quantitative real-time PCR (qRT-PCR). The values are shown as the mean ± SD of three independent experiments, n = 4 mice per group. (B) The protein levels of BCL-W, SAPK/JNK, and SMAC in the mice hippocampi were examined by western blotting, and the results were quantitatively analyzed. Results are presented as the mean ± SD, n = 3 mice per group *: p < 0.05, **: p < 0.01, ***: p < 0.001.
Fig 3: Amyloid-ß mediated the effect of T. denticola infection on neuronal apoptosis. (A) N2a cells were pretreated with KMI1303, then co-cultured with T. denticola, and the apoptosis rate was examined using TUNEL staining. (B) The protein levels of cleaved caspase-3, BCL-W, SAPK/JNK, and SMAC in N2a cells in each group were assessed by western blotting, and the results were quantitatively analyzed. Results are presented as the mean ± SD, *: p < 0.05, **: p < 0.01, ***: p < 0.001, n = 3 per experiment.
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