Inhibition of DNA Repair Protein Ku70 in High-Glucose Environment Aggravates the Neurotoxicity Induced by Bupivacaine in SH-SY5Y Cells.

ABSTRACT: Bupivacaine, a common local anesthetic, causes serious nerve injury, especially in diabetic patients, as high glucose has been reported to enhance bupivacaine-induced neurotoxicity. However, the key regulator for synergism remains unknown. To our surprise, the expression of repair protein Ku70 is suppressed, while the high-glucose environment induces DNA oxidative damage in neurons. Here, we aim to investigate whether the inhibition of Ku70 by high-glucose conditions aggrandized bupivacaine-induced DNA damage. Consistent with previous results, bupivacaine induced reactive oxygen species production and upregulated Ku70 and cleaved caspase-3 expressions at both transcript and protein levels and ultimately caused nucleic acid damage and apoptosis in human neuroblastoma (SH-SY5Y) cells. High-g

SUBMITTER: Ji ZH 

PROVIDER: S-EPMC7013357 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature