The potential neuroprotection efficacy of Atractylenolide III on kainic-acid derived temporal lobe epilepsy in male rats

Abstract

Purpose: Atractylenolide III (ATR III) is known for its anti-inflammatory and neuroprotective activities. In this study, we aimed to investigate the effects of ATR III on neuronal damage in temporal epileptic rats caused by kainic acid. Materials and Methods: 16-week-old Wistar Albino rats were divided into three groups; control (C, n=8), kainic acid (KA, n=8), ATR III+ kainic acid (KA+ATR, n=8). After 21 days of injections of kainic acid, learning, and memory behavior, anxiety, and locomotor activity were evaluated. Neuron morphologies in the hippocampus were examined, the total number of neurons, and the number of degenerated neurons were determined, and the thickness of these regions was also measured. Changes in biochemical parameters such as MDA, SOD, GSHPx, AChE, and CAT were investigated to detect oxidative stress in the brain. Results: There was no significant difference in the learning and memory function and locomotor activity. However, KA increased anxiety behavior without any effect of ATR III (closed arm duration, 244.90±25.17). There was no degeneration in the neurons of the control group. In the KA group, there was an increase in the number of degenerated neurons. In this group, the thicknesses in CA1, CA3, and DG regions were 37.39±1.90, 45.64±6.26 and 46.02±5.72 µm, respectively. In the ATR III+KA group, there were fewer degenerated neurons, less thinning of the hippocampus, and a higher number of normal neurons compared to the KA group. In this group, CA1, CA3, and DG thicknesses were calculated as 36.05±4.13, 47.09±7.09 and 43.07±5.91 µm, respectively. Conclusion: These findings suggest that ATR III may have the potential as a therapeutic agent for reducing neuronal damage in temporal epilepsy. Further research is warranted to explore the underlying mechanisms and evaluate the clinical implications of ATR III in the treatment of epilepsy.