Figure 4.

ProBiotic-4 alleviated the BBB injury and inflammationin aged SAMP8 mice. (A) Representative immunoblots and quantitative analysis of ZO-1, VE-cadherin, occludin, and claudin-5 expressions in the brain tissues. The levels of ZO-1, VE-cadherin, occludin, and claudin-5 were normalized to β-actin. The results are expressed as the normalized optical density value relative to the vehicle-treated SAMR1 group. (B) TEM observation of ultrastructure of the BBB. (C) Representative photomicrographs of Iba-1-positive microglia and GFAP-positive astrocytes in the hippocampal CA1 area. (D) Quantitative photomicrograph analysis of the Iba-1- and GFAP-positive area in the hippocampal CA1 area. (E) LPS level in the brain was measured by ELISA. (F) Representative immunoblots and quantitative analysis of TLR4 expression in the brain tissues. The levels of TLR4 were normalized to β-actin. The results are expressed as the normalized optical density value relative to the vehicle-treated SAMR1 group. (G) Representative immunoblots and quantitative analysis of the NF-κB nuclear translocation in the brain tissues. The levels of NF-κB were normalized to lamin B. The results are expressed as the normalized optical density value relative to the vehicle-treated SAMR1 group. (H) PCR analysis of Il-6 and Tnf-α mRNA levels in the brain. The relative mRNA levels of Il-6 and Tnf-α were normalized to Gapdh. The results are expressed as the normalized fold change relative to vehicle-treated SAMR1 group. The data are expressed as mean ± SEM (n = 5–6/group). *P < 0.05, **P < 0.01 versus SAMP8 group treated with vehicle (one-way ANOVA followed by the Tukey post hoc test).