ArticleMolecular neurobiology2025
3-Acetyl-11-Keto-β-Boswellic acid (AKBA) Attenuated 6-Hydroxydopamine (6-OHDA)-Induced Toxicity in SH-SY5Y Cells via Modulation of Akt/mTOR Pathway.
Article in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Ginkgolide B Attenuates 6-Hydroxydopamine-Induced Cellular Damage and Modulates Oxidant-Evoked CaCurrent issues in molecular biology · 2026Article
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4 authors.
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Abstract
One of the neurodegenerative diseases is Parkinson's, which is created due to the destruction of dopaminergic pathways in the brain. Different studies have proved the antioxidant, anti-inflammatory, and neuroprotective properties of Boswellia serrata. This study was designed to test the impact of 3-acetyl-11-keto-β-boswellic acid (AKBA) on toxicity induced by 6-hydroxydopamine (6-OHDA) in SH-SY5Y dopaminergic cells. SH-SY5Y cells were concurrently treated with different concentrations of AKBA (2.5, 5, 10, and 20 µM) and 6-OHDA (300 µM) for 24 h. The cells' viability, reactive oxygen species (ROS), and malondialdehyde (MDA) levels, as well as superoxide dismutase (SOD) activity, glutathione (GSH), and the apoptosis rate, were determined. The expressions of Akt/mTOR genes and the amounts of inflammatory parameters (TNF-α, IL-6, and IL-1β) were also evaluated using RT-PCR and ELISA methods, respectively. AKBA (2.5, 5, 10, 20 μM) significantly improved the viability of SH-SY5Y cells (p < 0.01) after 6-OHDA insult. The elevated amounts of ROS and MDA were also decreased (p < 0.05 for both) after treatment with AKBA. In the same way, the GSH content and SOD activity were significantly (p < 0.001) elevated by AKBA. AKBA (2.5 μM and 5 μM) also significantly (p < 0.001) prevented apoptosis and inhibited (p < 0.05) the release of proinflammatory cytokines (TNF-α, IL-6, and IL-1β) in 6-OHDA-treated SH-SY5Y cells. Besides, Akt/mTOR mRNA levels were decreased by 2.5 μM and 5 μM of AKBA (p < 0.05). AKBA improved the viability of the SH-SY5Y cells exposed to 6-OHDA by decreasing oxidative stress and the release of the pro-inflammatory cytokines and inhibited apoptosis through the decrease of Akt/mTOR expression. The obtained findings have enhanced our knowledge of the neuroprotective effects of AKBA. The present study offers novel insight into the impact of AKBA in modulating key pathological features of PD and underscores its potential as a clinically translatable agent for the development of effective neuroprotective therapies.
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