In vitro study reveals sea buckthorn improves lipid metabolism in psoriasis and NAFLD model, suggesting therapeutic potential.
Objective This study used an in vitro model based on HaCaT cells to investigate the mechanism of sea buckthorn ( Hippophae rhamnoides ) on psoriasis and cellular responses related to lipid metabolism disorders (for the observation of non-alcoholic fatty liver disease), focusing on phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/forkhead box O1 (FoxO1) signaling pathway. Methods Human immortalized keratinocyte cell line (HaCaT) cells were assigned into normal control (NC) group (cultured normally), interleukin (IL)-17 group (psoriasis model induced by 80 ng/L IL-17), triglyceride (TG) group (HaCaT cells treated with 0.15 g/L TG to induce lipid accumulation, establishing an in vitro cellular model of lipid stress associated with NAFLD), IL-17 + TG group (cellular model induced by combined IL-17 and TG), and IL-17 + TG + sea buckthorn -containing serum (SBCS) group (cellular model constructed using SBCS). Cell proliferation viability was evaluated with the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. Lipid profile markers were measured by enzymatic colorimetric assay. Cell apoptosis and cycle distribution were analyzed by flow cytometry. Levels of key components in the PI3K/AKT/FoxO1 pathway were determined by Western blotting. Results In comparison to the NC group, the IL-17 group exhibited increased cell proliferation and decreased apoptosis rate ( P < 0.05). The TG group exhibited elevated levels of TG and LDL, along with reduced HDL ( P < 0.05). Both the IL-17 and TG groups demonstrated G2/M phase cell cycle arrest, increased p-PI3K, p-AKT, and p-FoxO1 expressions ( P < 0.05). The alterations in all these indicators were more pronounced in the IL-17 + TG group relative to the individual model groups. In contrast, treatment with SBCS in the IL-17 + TG + SBCS group significantly reversed these changes relative to the IL-17 + TG group. Conclusion Sea buckthorn demonstrated significant therapeutic effects on the cellular model of psoriasis and NAFLD-related lipid metabolism stress. Its primary mechanism likely involves the effective suppression of the overactivated PI3K/AKT/FoxO1 pathway, thereby improving lipid metabolism and cellular function.
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Yin et al. (2026) studied this question.
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