Lycopene (LCP) is a carotenoid that protects against many diseases by alleviating oxidative stress. However, the effect of LCP on epileptic seizures has not been examined well in previous studies. In the current work, we employed kainic acid (KA) to induce experimental epileptic seizures in mice, and investigated the function of LCP during this process. We found that the onset and extent of KA-induced seizures were alleviated in LCP-pretreated mice. Nissl staining of hippocampus showed that the granule cell dispersion lesion induced by KA was improved by the LCP treatment. Additionally, we analyzed the oxidative stress levels in mice and found that LCP elevated SOD activity and suppressed MDA level in KA-induced seizures. Moreover, the expression of GABA receptors was influenced by LCP treatment. LCP suppressed the upregulation of gabrb2 and gabrb3 induced by KA, whereas it enhanced the expression of gabrb1. Results suggested that LCP plays a protective function in KA-induced seizures. Hence, it may be a potential functional food alternative for controlling and treating epileptic seizures.
Keywords: GABA receptors; Kainic acid; Lycopene; Oxidative stress; Seizures.
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