Brain and behavior · 2025
Anti-Apoptotic Effects of Escin on Porphyromonas gingivalis-Derived Lipopolysaccharide-Induced Injury in SH-SY5Y Cells.
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Sun Yingying, Zhang Rui, Pan Yunping, Sun Yufei, Liu Limin, Feng Min, Du Yuan, Wang Tian, Liu Shutai
Аннотация
BACKGROUND: Porphyromonas gingivalis-derived lipopolysaccharide (Pg-LPS) may be associated with the pathogenesis of Parkinson's disease and other neurodegenerative disorders. Escin is a bioactive compound found in the horse chestnut tree (Aesculus hippocastanum). This research investigated the impact of escin on Pg-LPS-induced injury in SH-SY5Y cells.
METHODS: Parkinson's disease model was established using SH-SY5Y neuronal cells. Cell viability was evaluated with MTT assays. Cell morphology was observed by fluorescence microscopy. Apoptosis was detected by JC-1, TUNEL, and Hoechst/propidium iodide staining, and flow cytometric analysis. The mRNA levels of BCL2 and BAX were determined by RT-PCR, and the protein levels of BCL2/BAX, cleaved Caspase 3/Caspase 3, and PARP were evaluated through Western blotting.
RESULTS: Escin mitigated the reduction in viability of SH-SY5Y cells caused by Pg-LPS. Pg-LPS triggered apoptosis in SH-SY5Y cells, alleviated by escin dose-dependently. Furthermore, the anti-apoptotic effect of escin was reversed by a specific apoptotic inducer.
CONCLUSIONS: Pg-LPS leads to SH-SY5Y cells' mitochondria malfunction and programed cell death. Escin alleviated SH-SY5Y cell injury induced by Pg-LPS through its anti-apoptotic effects.
METHODS: Parkinson's disease model was established using SH-SY5Y neuronal cells. Cell viability was evaluated with MTT assays. Cell morphology was observed by fluorescence microscopy. Apoptosis was detected by JC-1, TUNEL, and Hoechst/propidium iodide staining, and flow cytometric analysis. The mRNA levels of BCL2 and BAX were determined by RT-PCR, and the protein levels of BCL2/BAX, cleaved Caspase 3/Caspase 3, and PARP were evaluated through Western blotting.
RESULTS: Escin mitigated the reduction in viability of SH-SY5Y cells caused by Pg-LPS. Pg-LPS triggered apoptosis in SH-SY5Y cells, alleviated by escin dose-dependently. Furthermore, the anti-apoptotic effect of escin was reversed by a specific apoptotic inducer.
CONCLUSIONS: Pg-LPS leads to SH-SY5Y cells' mitochondria malfunction and programed cell death. Escin alleviated SH-SY5Y cell injury induced by Pg-LPS through its anti-apoptotic effects.