Medicine · 2025
Scutellarein attenuates alcohol-induced hepatocyte injury by modulating NF-κB and NRF2 signaling pathways.
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Shen Shuxia, Cao Minghua, Sui Ziqi
Аннотация
BACKGROUND: Alcohol-induced liver injury remains a major public health concern, and effective hepatoprotective agents are urgently needed. Scutellarein (SCU), a natural flavonoid, has shown potential biological activity, but its hepatoprotective effects and underlying mechanisms against alcohol-induced hepatocyte injury have not been fully elucidated.
METHODS: An in vitro model of alcohol-induced hepatocyte injury was established using human LO2 cells exposed to 400 mM alcohol. Cells were pretreated with 5 µM SCU, and multiple assays were performed to evaluate hepatocyte viability, hepatic enzyme activity, apoptosis, inflammatory cytokine expression, oxidative stress, and related signaling pathways.
RESULTS: SCU pretreatment effectively reversed the alcohol-induced reduction in cell viability and significantly lowered alanine aminotransferase and aspartate aminotransferase levels. SCU inhibited apoptosis by downregulating BAX and upregulating BCL2, and attenuated inflammatory responses by reducing interleukin-1β, interleukin-6, and tumor necrosis factor-alpha expression. Mechanistically, SCU suppressed nuclear factor kappa-B signaling by decreasing phosphorylation of p65 and inhibitor of nuclear factor kappa-Bα. In addition, SCU enhanced antioxidant defense by upregulating superoxide dismutase 1, superoxide dismutase 2, and catalase, and activating the nuclear factor erythroid 2-related factor 2-NAD(P)H quinone dehydrogenase 1 pathway.
CONCLUSION: SCU protects hepatocytes against alcohol-induced injury by modulating apoptosis, inflammation, and oxidative stress through regulation of nuclear factor kappa-B and nuclear factor erythroid 2-related factor 2 signaling pathways. These findings highlight its potential as a promising hepatoprotective agent.
METHODS: An in vitro model of alcohol-induced hepatocyte injury was established using human LO2 cells exposed to 400 mM alcohol. Cells were pretreated with 5 µM SCU, and multiple assays were performed to evaluate hepatocyte viability, hepatic enzyme activity, apoptosis, inflammatory cytokine expression, oxidative stress, and related signaling pathways.
RESULTS: SCU pretreatment effectively reversed the alcohol-induced reduction in cell viability and significantly lowered alanine aminotransferase and aspartate aminotransferase levels. SCU inhibited apoptosis by downregulating BAX and upregulating BCL2, and attenuated inflammatory responses by reducing interleukin-1β, interleukin-6, and tumor necrosis factor-alpha expression. Mechanistically, SCU suppressed nuclear factor kappa-B signaling by decreasing phosphorylation of p65 and inhibitor of nuclear factor kappa-Bα. In addition, SCU enhanced antioxidant defense by upregulating superoxide dismutase 1, superoxide dismutase 2, and catalase, and activating the nuclear factor erythroid 2-related factor 2-NAD(P)H quinone dehydrogenase 1 pathway.
CONCLUSION: SCU protects hepatocytes against alcohol-induced injury by modulating apoptosis, inflammation, and oxidative stress through regulation of nuclear factor kappa-B and nuclear factor erythroid 2-related factor 2 signaling pathways. These findings highlight its potential as a promising hepatoprotective agent.