Abstract
[Objective] To explore the protective effect and mechanism of a compound staple food (CSF ) against H2O2-induced oxidative damage in human hepatocellular carcinoma cells (HepG 2). [Methods] The in vitro antioxidant capacity of CSF was evaluated using DPPH and ABTS radical scavenging assays. An oxidative stress model was established by inducing HepG 2 cells with H2O2, and the effect of CSF on cell viability was measured by the CCK-8 assay. The impact of CSF on cellular oxidative stress was assessed by measuring reactive oxygen species (ROS ), mitochondrial membrane potential (JC-1), malondialdehyde (MDA ), and superoxide dismutase (SOD ) levels. The effect of CSF on apoptosis was detected by flow cytometry. Expression changes of oxidative damage-related proteins (Nrf2, HO-1, NQO-1, Bax, and Bcl-2) were analyzed by Western blot. [Results] CSF effectively scavenged DPPH and ABTS radicals. Compared with the model group, CSF treatment increased the viability of H2O2-induced HepG 2 cells, reduced ROS levels, slowed the decline of mitochondrial membrane potential, increased SOD activity, decreased MDA content, and alleviated Nrf 2 nuclear translocation. CSF treatment reduced the apoptosis rate by 8% compared with the model group. Western blot results showed that CSF upregulated the expression of Nrf 2, HO-1, and NQO-1, increased Bcl-2 levels, and downregulated Bax expression. [Conclusion] CSF improves H2O2-induced oxidative damage in HepG 2 |cells by activating the Nrf 2/HO-1 pathway and regulating the Bcl-2/Bax pathway.
Publication Date
11-19-2025
First Page
132
Last Page
140
DOI
10.13652/j.spjx.1003.5788.2024.81154
Recommended Citation
Beibei, NIE; Wu, LUO; Shengxiang, GUO; Shu, LIN; and Dongbo, LIU
(2025)
"Protective effect of a compound staple food against oxidative damage in HepG 2 cells,"
Food and Machinery: Vol. 41:
Iss.
10, Article 18.
DOI: 10.13652/j.spjx.1003.5788.2024.81154
Available at:
https://www.ifoodmm.cn/journal/vol41/iss10/18
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