12-Epi-Napelline Inhibits Leukemia Cell Proliferation via the PI3K/AKT Signaling Pathway In Vitro and In Vivo

Figure 5

IGF-1 attenuated the induction of apoptosis by 12-epi-napelline. K-562 and HL-60 cells were pretreated with IGF-1 (100 ng/ml) for 2 h followed by 12-epi-napelline for 24 h Apoptosis was determined by flow cytometry. (a, c) Typical flow cytometric graph of apoptosis. (b, d) The average percentage of apoptosis in K-562 and HL-60 cells after treatment with 12-epi-napelline. (e) The expression of PI3K, AKT, p-AKT, mTOR, caspase-3, cleaved caspase-3, caspase-9, and Bcl-2 was detected by western blot. The results showed that IGF-1 partly prevented 12-epi-napelline-induced apoptosis and attenuated the repressive effect of 12-epi-napelline on PI3K, AKT, p-AKT, and mTOR in K-562 and HL-60 cells. IGF-1: insulin-like growth factor 1; E: 12-epi-napelline; IGF-1+E: insulin-like growth factor 1 + 12-epi-napelline. (and compared to the control, n = 3).

(a)

(b)

(c)

(d)

(e)