Cichorium Endivia ve Urtica Dioica Ekstraktlarının SH-SY5Y Hücrelerinde H2O2 Kaynaklı Strese Karşı Etkisi

Yıl 2024, Sayı: 23, 538 - 553, 31.08.2024

Hatice Feyzan Ay , Serap Yeşilkır Baydar , Rabia Çakır Koç

https://doi.org/10.38079/igusabder.1428159

Öz

Amaç: Nörodejeneratif hastalıklarda artan hidrojen peroksit (H2O2) üretimi nöronlarda oksidatif strese neden olur ve hasar şiddetli olduğunda geri dönüşümsüz olur ve apoptoz tetiklenir. Son yıllarda nöronları oksidatif stresten korumak için nöroprotektif ve antioksidan özellikler sergileyen fitokimyasallar önem kazanmıştır. Bu nedenle yüksek antioksidan kapasitesine ve anti-apoptotik özelliklere sahip bitkisel ekstraktlar H2O2 indüksiyonuna karşı koruyucu bir strateji sağlayabilmektedir. Bu çalışma, Cichorium endivia sıvı ekstraktının (CEE) ve Urtica dioica sıvı ekstraktının (UDE) SH-SY5Y hücreleri üzerindeki H2O2 indüksiyonuna karşı in vitro etkisini incelemeyi amaçlamaktadır.
Yöntem: Bu amaçla hücreler ekstraktlarla muamele edildikten sonra H2O2'ye maruz bırakıldı. Bu ekstraktların nöroprotektif etkisi ve hücre canlılığı XTT yöntemi ile değerlendirildi. Antioksidan aktivite CUPRAC yöntemiyle belirlendi. Son olarak ise apoptotik hücre ölümü ve reaktif oksijen türleri (ROS) düzeyi sırasıyla DAPI ve DCFH-DA ile incelendi.
Bulgular: Elde edilen sonuçlar, CEE ve UDE'nin H2O2 kaynaklı toksisiteyi, apoptotik hücre ölümünü ve ROS düzeylerini azaltarak nöroproteksiyon, anti-apoptotik ve antioksidan etkiler üzerinde etkiye sahip olduğunu gösterdi.
Sonuç: H2O2 oksidatif hasar yoluyla nöronlarda nörotoksisiteye neden olmaktadır. Bunu önlemek amacıyla yüksek antioksidan aktiviteye sahip geleneksel bitki ekstraktları nöroprotektif bir strateji sağlayabilmektedir. Sonuç olarak in vitro modelde bu bitkisel ekstraktların nöroprotektif etki sergileyebileceği gösterilmiştir.

Anahtar Kelimeler

Cichorium endivia, Urtica dioica, nöroprotektif etki, nörotoksisite, oksidatif hasar, hidrojen peroksit (H2O2)

Proje Numarası

KAP-270320-SYB

The Influence of Cichorium Endivia and Urtica Dioica Extracts Against H2O2-Induced Stress in SH-SY5Y Cells

Öz

Aim: In neurodegenerative diseases, increased production of hydrogen peroxide (H2O2) causes oxidative stress in neurons, and when the damage is severe, it is irreversible and apoptosis is induced. In recent years, phytochemicals that exhibit neuroprotective and antioxidant properties to protect neurons from oxidative stress have gained importance. Therefore, herbal extracts with high antioxidant capacity and anti-apoptotic properties may provide a protective strategy against H2O2-induction. This study aims to examine the influence of Cichorium endivia liquid extract (CEE) and Urtica dioica liquid extract (UDE) against H2O2-induction on SH-SY5Y cells in vitro.
Method: For this purpose, cells were treated with the extracts and then exposed to H2O2. The neuroprotective effect and cell viability of these extracts were evaluated by XTT method. Antioxidant activity was determined by the CUPRAC method. Finally, the apoptotic cell death and reactive oxygen species (ROS) levels were examined with DAPI and DCFH-DA, respectively.
Results: The results obtained showed that CEE and UDE have an influence on neuroprotection, anti-apoptotic, and antioxidant effects by reducing H2O2-induced toxicity, apoptotic cell death, and ROS levels.
Conclusion: H2O2 causes neurotoxicity in neurons through oxidative damage. To prevent this, traditional plant extracts with high antioxidant activity can provide a neuroprotective strategy. As a consequence, it was shown in an in vitro model that these herbal extracts could be a neuroprotective effect.

Anahtar Kelimeler

Cichorium endivia, Urtica dioica, neuroprotective effect, neurotoxicity, oxidative damage, hydrogen peroxide (H2O2)

Destekleyen Kurum

This study has been funded by Istanbul Gelişim University Scientific Research Projects Application and Research Center and carried out at Yıldız Technical University.

Proje Numarası

KAP-270320-SYB

Teşekkür

This study has been funded by Istanbul Gelişim University Scientific Research Projects Application and Research Center. Project number: KAP-270320-SYB.

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