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