Neuroprotective Potential of Boric Acid in a Rotenone-induced in Vitro Parkinson’s Disease Model
Lokman Hekim health sciences (Online), cilt.6, sa.4, ss.721-729, 2026 (TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 6 Sayı: 4
- Basım Tarihi: 2026
- Doi Numarası: 10.14744/lhhs.2026.89749
- Dergi Adı: Lokman Hekim health sciences (Online)
- Derginin Tarandığı İndeksler: Central & Eastern European Academic Source (CEEAS), CINAHL, Directory of Open Access Journals, TR DİZİN (ULAKBİM)
- Sayfa Sayıları: ss.721-729
- Dokuz Eylül Üniversitesi Adresli: Evet
Özet
Introduction: Parkinson’s disease (PD) is characterized by progressive dopaminergic neurodegeneration and pathological α-synuclein aggregation. Mitochondrial dysfunction and oxidative stress are central to PD pathogenesis, and mitochondrial complex I inhibitors such as rotenone are widely used to model PD-related neurotoxicity in vitro. Boric acid (BA), a boron-containing compound with reported antioxidant and neuroprotective properties, has not been fully explored in PD-related apoptotic mechanisms. Therefore, this study aimed to investigate the neuroprotective and anti-apoptotic effects of BA in a rotenone-induced in vitro PD model using SH-SY5Y human neuroblastoma cells. Methods: SH-SY5Y cells were exposed to 50 μM rotenone to induce PD-like neurotoxicity and co-treated with BA at concentrations ranging from 100 to 800 μM. Cell viability was assessed using the 3-(4,5-dimethylthiazol-2-yl)-2,5- diphenyltetrazolium bromide assay. Apoptosis-related molecular changes were evaluated by real-time quantitative polymerase chain reaction and Western blot analyses, focusing on key regulators of mitochondrial apoptosis, including BAX (B-cell lymphoma 2 [BCL-2]-associated X protein), BCL-2, and cleaved caspase-3. Results: Rotenone treatment significantly reduced cell viability compared to control cells. Co-treatment with 200 μM BA markedly restored cell viability (**p<0.01), indicating a strong neuroprotective effect. Molecular analyses demonstrated that BA treatment significantly decreased the BAX/BCL-2 ratio in rotenone-treated cells (p=0.0295), suggesting an attenuation of mitochondria-mediated apoptotic signaling. Discussion and Conclusion: These findings demonstrate that BA exerts a significant neuroprotective effect against rotenone-induced cytotoxicity by enhancing cell survival and modulating apoptosis-related pathways. BA may represent a promising candidate for mitigating PD-associated neuronal damage, warranting further mechanistic and in vivo investigations.