Mitochondrial kinetic mechanism by which triptolide alleviates hydrogen peroxide-induced apoptosis in SH-SY5Y cells

doi:10.12307/2026.892

Abstract

Abstract: BACKGROUND: Previous studies from our group have shown that triptolide exerts protective effects on nerve cells and alleviates symptoms of neurodegenerative diseases. However, whether it acts by improving mitochondrial dynamic abnormalities requires further investigation.
OBJECTIVE: To explore the effect and mechanism of triptolide in regulating the mitochondrial fusion-fission balance to mitigate hydrogen peroxide (H₂O₂)-induced apoptosis in SH-SY5Y cells.
METHODS: Human neuroblastoma SH-SY5Y cells were cultured and divided into three groups: control group, model group (200 μmol/L H₂O₂), and triptolide group (2.5 nmol/L triptolide + 200 μmol/L H₂O₂). After 24 hours of intervention, oxidative stress markers (superoxide dismutase activity and malondialdehyde levels), mitochondrial membrane potential, and apoptotic rate were measured. Western blot was used to detect the expression of apoptosis-related proteins, mitochondrial dynamics-related proteins, and respiratory chain-related proteins. Immunofluorescence staining was used to detect the expression of phospho-dynamin-related protein 1, optic atrophy protein 1, cytochrome c oxidase 1, and ATP synthase F1 subunit α.
RESULTS AND CONCLUSION: Compared with the control group, the model group showed significantly decreased superoxide dismutase activity, mitochondrial membrane potential, and expression levels of anti-apoptotic protein Bcl-2, mitochondrial fusion protein 1, mitochondrial fusion protein 2, optic atrophy protein 1, and ubiquinone oxidoreductase subunit B8, panthenol-cytochrome C reductase core protein 2, cytochrome C oxidase 1, succinate dehydrogenase B, and ATP synthase F1 subunit α (P < 0.05). In contrast, malondialdehyde levels, expression of pro-apoptotic proteins (Bax, Caspase-3) and mitochondrial fission protein 1 and phospho-p161, and apoptotic rate were significantly increased (P < 0.05). Compared with the model group, triptolide intervention reduced malondialdehyde levels, increased superoxide dismutase activity and mitochondrial membrane potential, promoted the expression of fusion proteins, suppressed the expression of fission proteins, elevated the levels of oxidative phosphorylated complex protein, and decreased the apoptotic rate (P < 0.05). These results confirm that triptolide can alleviate H₂O₂-induced apoptosis in SH-SY5Y cells by regulating mitochondrial dynamic imbalance.

Key words: triptolide, oxidative stress, neuron, apoptosis, mitochondrial dynamic balance, oxidative phosphorylation

CLC Number:

Mu Bingtao, Guo Minfang, Hu Fenqi, Liu Qiyuan, Jia Hui, Xu Mingyuan, Chen Jiayuan, Zhang Huiyu, Meng Tao, Yu Jiezhong. Mitochondrial kinetic mechanism by which triptolide alleviates hydrogen peroxide-induced apoptosis in SH-SY5Y cells[J]. Chinese Journal of Tissue Engineering Research, 2026, 30(34): 8986-8993.

Figures/Tables 5

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