Figure 4. The upstream components of mitochondria-mediated caspase-dependent apoptotic pathway in a normotensive Wistar Kyoto (WKY) group, a spontaneously early aged hypertensive (SHR) group and a hypertension with 12 weeks exercise training (SHR-EX) group. (A) The representative protein levels of t-Bid (BH3 interacting domain death agonist), Bax (Bcl-2 Associated X), Bak (Bcl-2-agonist/killer 1), Bad (Bcl-2 agonist cell death) as well as Bcl-2, Bcl-xL, p-Bad, and 14-3-3 proteins extracted from western blotting analysis. The α-tubulin was used as an internal control. (B, C) Bars represent the cerebral cortices of excised brain in WKY, SHR, and SHR-EX groups were measured by Wt the pro-apoptotic as well as pro-survival relative fold changes of protein quantification relative to the control group in t-Bid, Bax/Bcl-2, Bak/Bcl-xL as well as pBad/Bad pBad and 14-3-3 on α-tubulin, respectively, and mean values ± SD (n=6 in each group). *: p<0.05, **: p<0.01, in comparison between SHR and WKY rat group; ##: p<0.01, ###: p<0.001 in comparison between SHR-EX group and SHR group.