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

Yıl 2024, Cilt: 49 Sayı: 2, 446 - 459, 30.06.2024

Hüsniye Özalp , Yusuf Çamlıca , Leyla Şahin , Savaş Aktaş , Serap Yalın , Metin Yıldırım , Ayla Batu Öztürk , Özge Selin Çevik

https://doi.org/10.17826/cumj.1401169

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

Atractylenolide III'ün erkek sıçanlarda kainik asit kaynaklı temporal lob epilepsisi üzerindeki potansiyel nörokoruyucu etkinliği

Öz

Amaç: Atractilenolide III'ün (ATR III) antiinflamatuar ve nöroprotektif aktiviteleri olduğu bilinmektedir. Bu çalışmada ATR III' ün temporal epileptik sıçanlarda kainik asidin neden olduğu nöronal hasar üzerine etkilerini araştırmayı amaçladık.
Gereç ve Yöntem: 16 haftalık Wistar Albino sıçanları; kontrol (C, n=8), kainik asit (KA, n=8), ATR III+ kainik asit (KA+ATR, n=8) olacak şekilde üç gruba ayrıldı. 21 günlük kainik asit enjeksiyonundan sonra öğrenme ve hafıza davranışı, anksiyete ve lokomotor aktivite değerlendirildi. Hipokampustaki nöron morfolojileri incelendi, toplam nöron sayısı, dejenere nöron sayısı belirlendi ve bu bölgelerin kalınlıkları da ölçüldü. Beyindeki oksidatif stresi tespit etmek amacıyla MDA, SOD, GSHPx, AChE ve CAT gibi biyokimyasal parametrelerdeki değişiklikler araştırıldı.
Bulgular: Öğrenme ve hafıza fonksiyonu ile lokomotor aktivitede anlamlı bir fark yoktu. Ancak KA, ATR III' ün herhangi bir etkisi olmadan kaygı davranışını artırdı (Kapalı kolda geçirilen süre, 244.90±25.17). Kontrol grubunun nöronlarında herhangi bir dejenerasyon görülmedi. KA grubunda dejenere nöron sayısında artış görüldü. Bu grupta CA1, CA3 ve DG bölgelerindeki kalınlıklar sırasıyla 37,39±1,90, 45,64±6,26 ve 46,02±5,72 µm idi. ATR III+kainik asit grubunda, KA grubuna kıyasla daha az dejenere nöron, hipokampusta daha az incelme ve daha fazla sayıda normal nöron vardı. Bu grupta CA1, CA3 ve DG kalınlıkları sırasıyla 36,05±4,13, 47,09±7,09 ve 43,07±5,91 µm olarak hesaplandı.
Sonuç: Bu bulgular ATR III'ün temporal epilepside nöronal hasarı azaltmak için terapötik bir ajan olarak bir potansiyele sahip olduğunu göstermektedir. Altta yatan mekanizmaları araştırmak ve ATR III'ün epilepsi tedavisindeki klinik etkilerini değerlendirmek için daha fazla sayıda araştırmaya ihtiyaç duyulmaktadır.

Anahtar Kelimeler

Hipokampus, epilepsi, atractylenoloide iii, kainik asit, oksidatif stres

Etik Beyan

Mersin Üniversitesi Lisansüstü Eğitim-Öğretim Yönetmeliğinde belirtilen kurallara uygun olarak hazırladığım bu tez çalışmasında, - Tez içindeki bütün bilgi ve belgeleri akademik kurallar çerçevesinde elde ettiğimi, - Görsel, işitsel ve yazılı tüm bilgi ve sonuçları bilimsel ahlâk kurallarına uygun olarak sunduğumu, - Başkalarının eserlerinden yararlanılması durumunda ilgili eserlere bilimsel normlara uygun olarak atıfta bulunduğumu, - Atıfta bulunduğum eserlerin tümünü kaynak olarak kullandığımı, - Kullanılan verilerde herhangi bir tahrifat yapmadığımı, - Bu tezin herhangi bir bölümünü Mersin Üniversitesi veya başka bir üniversitede başka bir tez çalışması olarak sunmadığımı, - Tezin tüm telif haklarını Mersin Üniversitesi’ne devrettiğimi beyan ederim.

Destekleyen Kurum

Mersin Üniversitesi, Bilimsel Araştırmalar Birimi

Proje Numarası

2019 2-TP2 3507

Teşekkür

This study was supported by Mersin University BAP unit with the code 2019 2-TP2 3507.

Kaynakça

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