Abstract:
Diclofenac is a non-steroidal anti-inflammatory drug that is prescribed for treatment of rheumatic diseases and
as an analgesic. Although the information about these side effects has been widely reported, little is know about the effect of diclofenac on the neural cells. In this study, we investigated the effects of diclofenac on the
proliferation and differentiation of PC12 cells. The cell proliferation was evaluated by using XTT assay in the
both free-serum neurobasal medium supplemented with B27 supplement and DMEM/F12 medium containing
10% FBS. The nerve growth factor (NGF)–induced differentiation was assessed by measuring the neurite
length. The drug toxicity was exhibited at the concentrations more than 310 µM in the supplemented neurobasal medium. The treatment of cells in the DMEM/F12 medium increased their sensitivity to diclofenac, with 40% and 75% growth inhibition at the 155 and 310 µM concentrations, respectively. The NGF-induced
differentiation was not reduced by toxic and subtoxic concentrations of diclofenac. The results of this study
indicated that diclofenac may be able to exhibit its neurotoxic effects through growth inhibition, but not
differentiation inhibition. Supplement of B27 has several antioxidant compounds. Therefore, the difference of
diclofenac cytotoxic effects in two culture media suggest that drug cytotoxicity may be related to the oxidative
stress.
