The DNA Repair Enzyme XPD Is Partially Regulated by PI3K/AKT Signaling in the Context of Bupivacaine-Mediated Neuronal DNA Damage

Figure 5

Inhibition of PI3K/AKT aggravated SH-SY5Y injury caused by bupivacaine and further increase the expression of XPD. Treatment with LY294002, a PI3K/AKT inhibitor, alone significantly increased XPD expression in SH-SY5Y cells ((a, b) ; ). Moreover, the expression of XPD was further increased in the bupivacaine and LY294002-treated group compared with the bupivacaine-treated group ((a, b) ; ^&) (^# vs. the control group). LY294002 (10 μM) further inhibited the protein expression of p-PI3K ((c, d) ; ^#) ( vs. the control group) and p-AKT ((c, e) ; ^#) ( vs. the control group) after bupivacaine treatment. The expression of the apoptosis-related proteins Bax and Bcl-2 and p-γH2AX (markers of DNA damage) was increased in the 10 μM LY294002 and bupivacaine-treated group compared with the bupivacaine group ((f) ^#; (g) ; ^#) ((f) vs. the control group) ((g) vs. the control group). The data are shown as the of three independent experiments.

(a)

(b)

(c)

(d)

(e)

(f)

(g)