The potential neuroprotection efficacy of Atractylenolide III on kainic-acid derived temporal lobe epilepsy in male rats
Öz
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.
Anahtar Kelimeler
Hippocampus, Epilepsy, Atractylenoloide III, Kainic acid, Oxidative stress
Proje Numarası
2019 2-TP2 3507
Kaynakça
- Novak A, Vizjak K, Rakusa M. Cognitive impairment in people with epilepsy. J Clin Med. 2022;11:267.
- Asadi-Pooya AA, Stewart GR, Abrams DJ, Sharan A. Prevalence and incidence of drug-resistant mesial temporal lobe epilepsy in the United States.World Neurosurg. 2017;99:662-6.
- Sarsılmaz A. Tek taraflı mezial temporal sklerozda karşı taraf hipokampüsün volüm değerlendirmesi. Bakırköy Tıp Dergisi. 2019;15:41-6.
- Aldenkamp AP, Overweg J, Gutter TH, Beun AM, Diepman L, Mulder OG. Effect of epilepsy, seizures and epileptiform EEG discharges on cognitive function. Acta Neurol. Scand. 1996;93:253-59.
- Miltiadous P, Stamatakis A, Koutsoudaki PN, Tiniakos DG, Stylianopoulou F. IGF-I ameliorates hippocampal neurodegeneration and protects against cognitive deficits in an animal model of temporal lobe epilepsy. Exp. Neurol.2011;231:223-35.
- Wahab A. Difficulties in treatment and management of epilepsy and challenges in new drug development.Pharmaceuticals. 2010;3:2090-110.
- Li Q, Chen XY, He L, Zhou D. Traditional Chinese medicine for epilepsy. Cochrane Database Syst. Rev.2009;3:CD006454..
- Wang J, Wong YK, Liao F. What has traditional Chinese medicine delivered for modern medicine? Expert Rev Mol Med. 2018;20:4.
- Zhao Z, He X, Ma C, Wu S, Cuan Y, Sun Y et al. Excavating anticonvulsant compounds from prescriptions of traditional Chinese medicine in the treatment of epilepsy. Am J Chin Med. 2018;46:707-37.
- Gong WX, Zhou YZ, Qin XM, DU GH. Involvement of mitochondrial apoptotic pathway and MAPKs/NF-κ B inflammatory pathway in the neuroprotective effect of atractylenolide III in corticosterone-induced PC12 cells. Chin J Nat Med. 2019;17:264-74.
