{'fraction_non_alphanumeric': 0.0326975476839237, 'fraction_numerical': 0.01226158038147139, 'mean_word_length': 5.068870523415978, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Propofol pretreatment prevents oxygen-glucose deprivation/reoxygenation(OGD/R)-induced inflammation through nuclear transcription factor κB (NF-κB) pathway in neuroblastoma cells.

BACKGROUND
Inflammation is one of the causes of neuroblastoma progression. Propofol attenuates inflammation by repressing nuclear transcription factor κB (NF-κB) in different diseases.But its effect on oxygen-glucose deprivation/reoxygenation (OGD/R)-induced inflammation is not known.


OBJECTIVE
This study investigated the role and mechanism of action of propofol on OGD/R-induced inflammation in mouse N2A neuroblastoma cells.


METHODS
MTT was performed on mouse neuroblastoma cells N2A to assess and select the maximum safe dose of propofol. Next, N2A cells were pretreated with propofol and then, exposed to the OGD condition for 3 h and reoxygenated for 6 h. The content of the inflammatory factors interleukin-1 beta (IL-1β) and tumor necrosis factor alpha (TNF-α) in the medium was measured by ELISA, while their protein expression was detected by western blot and immunofluorescence. The protein expression of P65, p-P65, IKBα and p-IKBα belonging to the NF-κB pathway was also determined by western blot in N2A cells. To further confirm the mechanism of propofol on OGD/R-induced inflammation in mouse N2A cells, P65 was over-expressed and the above experiments were repeated.


RESULTS
Propofol did not affect the cell viability of N2A cells even at the maximum concentration used (30 µM), thus, 30 µM of propofol was selected to perform our experiments. Besides, OGD/R induced inflammation and activation of NF-κB pathway with increased p-P65 and p-IKBα expression, and propofol pretreatment inhibited OGD/R induced inflammation and activation of NF-κB pathway in N2A cells. Over-expression of P56 abolished the effects of propofol on OGD/R-induced inflammation and activation of NF-κB pathway in N2A cells.


CONCLUSION
Our work demonstrated for the first time that propofol pretreatment ameliorated OGD/R induced inflammation via NF-κB pathway modulation in mouse neuroblastoma N2A cells, indicating propofol might be considered as a potential therapeutic approach to reduce inflammation in neuroblastoma.