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Dergiler / Journal of Basic and Clinical Health Sciences / 2026 / Volume: 10 Issue: 3

Boldine Exerts Neuroprotective Effects Against Rotenone Toxicity in SH-SY5Y In Vitro Model

Ferit Anıl Kocabaş(EGE UNIVERSITY, EGE FACULTY OF MEDICINE)0000-0002-8782-4357
Mümin Alper Erdoğan(İZMİR KATİP ÇELEBİ ÜNİVERSİTESİ, TIP FAKÜLTESİ)0000-0003-0048-444X
Özlem Yılmaz(Ege Üniversitesi Tıp Fakültesi Fizyoloji AD.)0000-0001-5744-0937
Sayfa
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Yayın Tarihi
2026-09-30
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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

Bulgular: Rotenon (200 nM), hücre canlılığını anlamlı olarak %32.3’e düşürdü, klonojenik potansiyeli azalttı (%3.9) ve aktif kaspaz-3 düzeylerini artırdı (p<0.0001). 0.1 µM boldin ile ön işlem, hücre canlılığını belirgin şekilde %92.2’ye ve klonojenik aktiviteyi %81.9’a yükseltirken, kaspaz-3 düzeylerini ve apoptotik nükleer değişiklikleri anlamlı olarak azalttı (p<0.0001).

📌 3 Maddede Bu Makale

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Amaç & Hipotez:Amaç: Rotenon, mitokondriyal işlev bozukluğu, oksidatif stres ve apoptoz yoluyla Parkinson hastalığı benzeri nörotoksisiteye neden olmaktadır.
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Temel Bulgular & Veri:Bu çalışmada, boldinin insan SH-SY5Y nöroblastoma hücrelerinde rotenon kaynaklı sitotoksisiteye karşı nöroprotektif etkinliği araştırıldı.
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Sonuç & Katkı:Bulgular: Rotenon (200 nM), hücre canlılığını anlamlı olarak %32.3’e düşürdü, klonojenik potansiyeli azalttı (%3.9) ve aktif kaspaz-3 düzeylerini artırdı (p<0.0001). 0.1 µM boldin ile ön işlem, hücre canlılığını belirgin şekilde %92.2’ye ve klonojenik aktiviteyi %81.9’a yükseltirken, kaspaz-3 düzeylerini ve apoptotik nükleer değişiklikleri anlamlı olarak azalttı (p<0.0001).
🔬Tür:Laboratuvar & Saha Deneyi
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Boldine · Rotenone · SH-SY5Y

Özet

Amaç: Rotenon, mitokondriyal işlev bozukluğu, oksidatif stres ve apoptoz yoluyla Parkinson hastalığı benzeri nörotoksisiteye neden olmaktadır. Bu çalışmada, boldinin insan SH-SY5Y nöroblastoma hücrelerinde rotenon kaynaklı sitotoksisiteye karşı nöroprotektif etkinliği araştırıldı. Gereç ve Yöntem: SH-SY5Y hücreleri, 200 nM rotenona 24 saat süreyle maruz bırakılmadan önce 2 saat boyunca boldin (0.1–100 µM) ile ön işleme tabi tutuldu. Hücre canlılığı, klonojenik kapasite, aktif kaspaz-3 düzeyleri ve apoptotik nükleer morfoloji sırasıyla MTS testi, klonojenik analiz, ELISA ve Hoechst 33342 boyaması kullanılarak değerlendirildi. Bulgular: Rotenon (200 nM), hücre canlılığını anlamlı olarak %32.3’e düşürdü, klonojenik potansiyeli azalttı (%3.9) ve aktif kaspaz-3 düzeylerini artırdı (p<0.0001). 0.1 µM boldin ile ön işlem, hücre canlılığını belirgin şekilde %92.2’ye ve klonojenik aktiviteyi %81.9’a yükseltirken, kaspaz-3 düzeylerini ve apoptotik nükleer değişiklikleri anlamlı olarak azalttı (p<0.0001). Daha yüksek boldin konsantrasyonları (≥5 µM) antiproliferatif etkiler gösterdi. Sonuç: Boldin, rotenon kaynaklı nörotoksisiteye karşı konsantrasyona bağlı bifazik bir yanıt göstermekte; düşük konsantrasyonlarda belirgin nöroprotektif, daha yüksek konsantrasyonlarda ise antiproliferatif etkiler sergilemektedir. 0.1 µM boldinin koruyucu etkisi, kaspaz-3 aktivasyonunun ve apoptotik nükleer değişikliklerin azalması ile ilişkili bulunmuştur.

Abstract

Purpose: Rotenone induces Parkinson's disease-like neurotoxicity through mitochondrial impairment, oxidative stress, and apoptosis. We investigated the neuroprotective efficacy of boldine against rotenone-induced cytotoxicity in human SH-SY5Y neuroblastoma cells. Material and Methods: SH-SY5Y cells were pretreated with boldine (0.1–100 µM) for 2 h before exposure to 200 nM rotenone for 24 h. Cell viability, clonogenic capacity, active caspase-3 levels, and apoptotic nuclear morphology were evaluated using the MTS assay, clonogenic assay, ELISA, and Hoechst 33342 staining, respectively. Results: Rotenone (200 nM) significantly reduced viability to 32.3%, suppressed clonogenic potential (3.9%), and increased active caspase-3 levels (p<0.0001). Pretreatment with 0.1 μ"M" boldine markedly restored cell viability to 92.2% and clonogenic activity to 81.9%, while significantly reducing caspase-3 levels and nuclear apoptotic alterations (p<0.0001). Higher boldine concentrations (≥5 μ"M" ) exhibited antiproliferative effects. Conclusion: Boldine exhibits a concentration-dependent biphasic response against rotenone-induced neurotoxicity, with marked neuroprotection at low concentrations and antiproliferative effects at higher concentrations. The protective effect of 0.1 µM boldine was associated with attenuation of caspase-3 activation and apoptotic nuclear alterations.

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Bu Makaleye Atıf Yap

Kocabaş, F. A., Erdoğan, M. A., Yılmaz, Ö. (2026). Boldine Exerts Neuroprotective Effects Against Rotenone Toxicity in SH-SY5Y In Vitro Model. Journal of Basic and Clinical Health Sciences, Volume: 10 Issue: 3. https://doi.org/10.30621/jbachs.2018841

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