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. 2017 Feb 25;13(3):327–338. doi: 10.7150/ijbs.17751

Figure 8.

Figure 8

ERK and PI3K/AKT/mTOR were involved in CP protecting pBVECs and up-regulating HIF-1a. CP (49 μg/ml) activated both ERK and mTOR to increase pS6K and p4EBP1. Inhibiting either ERK (by PD98059) or mTOR (by rapamycin) resulted in decreases in pS6K, p4EBP1, HIF-1a, mitochondrial Cyt-C and an increase in cytoplastic Cyt-C (A). (B) indicates that CP activating mTOR was dependent on PI3K/AKT but not ERK. (C)-(k) are statistical analysis of (A) and (B). (L) shows that inhibiting ERK or mTOR induced increases in apoptotic cells and necrotic cells as well as a decrease in cell viability. For apoptotic cell and necrotic cell, n = 6, mean ± SD; for western blot, n = 3, mean ± SD. * p<0.05; ** p<0.01; *** p<0.001.