Oxidative Medicine and Cellular Longevity / 2021 / Article / Fig 4

Research Article

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

Figure 4

Downregulation of XPD expression further aggravated the neurotoxicity caused by bupivacaine. After XPD expression was downregulated with the XPD-GV211-RNAi-expressing lentivirus, the SH-SY5Y cell apoptosis and DNA damage induced by bupivacaine were exacerbated. GV211-NC served as a control lentivirus. DNA damage was aggravated in bupivacaine-treated SH-SY5Y cells in which XPD expression was inhibited (Bup-GV211-RNAi) compared to the control group (Bup-GV211-NC), as the phosphorylation of γ-H2AX, a DNA damage marker, was significantly increased ((a, b) ; &), (, and #, vs. the control group). Furthermore, the expression of the apoptosis-related proteins Bcl-2 and Bax was reduced ((a, c) ; &) (, and # vs. the control group), and the olive tail moment was significantly higher in the comet assay ((d, e) ; &) (, and # vs. the control group). Moreover, suppression of XPD expression significantly increased the apoptosis ratio, as determined by flow cytometry ((f, g) ; &) (, and # vs. the control group). The data are shown as the of three independent experiments.

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