Oxidative Medicine and Cellular Longevity / 2021 / Article / Fig 1

Research Article

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

Figure 1

Bupivacaine causes neurotoxic damage. In vivo, bupivacaine-induced apoptotic damage in rat spinal cord tissue and behavioral changes. The rats in the neuronal damage model group were intrathecally administered 20 μL of 3% bupivacaine, while rats in the control group were administered normal saline. Twenty-four hours after treatment with bupivacaine, the TUNEL staining was performed to determine the cell apoptosis rate ((a, b) ; ) in spinal cord tissue slices. NeuN was used to label mature neurons. TUNEL/NeuN positive cells (a) represent apoptotic neurons. The PWMT and PWTL were increased in the bupivacaine-treated group compared with the control group ((c, d) ; ). The in vivo data are shown as the . Bupivacaine may induce SH-SY5Y cell neurotoxicity in vitro. After SH-SY5Y cells were exposed to different concentrations of bupivacaine, the dose inhibition curve was plotted ((e) ), and the IC50 of bupivacaine was calculated as 1.5 mmol/L. The release of LDH was determined to assess cytotoxicity ((f) ; and vs. the control group). The data are shown as the .
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