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/Rinduced
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
Results: Propofol did not affect 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/Rinduced
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 that propofol might be considered as a potential therapeutic approach to reduce inflammation