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.
Yin et al. (Fri,) studied this question.