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Diclofenac sodium is one of the commonly used therapeutic non-steroidal anti-inflammatory drugs; notwithstanding, diverse adverse effects are clearly described. In humans, vitamin C is an essential nutrient that is ubiquitously a water-soluble electron donor with biological characteristics. To a greater extent, it has been widely recognized not only as an antioxidant but also as a specific co-factor in patho-enzymatic processes and reactions. This study investigated the effect of vitamin C on the medial prefrontal cortex (mPFC) of juvenile mice exposed to Diclofenac sodium. Thirty juvenile mice were randomly assigned into 5 experimental groups; control, saline-treated, vitamin C treated, Diclofenac sodium treated, and vitamin C + Diclofenac sodium. Histochemical, immunohistochemical, stereologi-cal, and quantitative neurochemical studies were respectively, employed to assess the effect of vitamin C on Diclofenac sodium-associated neurological damage. Results showed that the histoarchitectural profile of the mPFC was well preserved in the control, saline, vitamin C, and vitamin C + Diclofenac sodium treated groups compared with the Diclofenac sodium treated group. Exposure to Diclofenac sodium during elicited significant glutamate level reduction in the mPFC. Furthermore, co-administration of vitamin C + Diclofenac sodium significantly decreased (p<0.05) glutamate level compared with the Diclofenac sodium-treated group. It could be concluded from this study that vitamin C conferred neuroprotective effect on the mPFC of the juvenile mice exposed to Diclofenac sodium.

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