Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
[Cajanonic acid A derivative XJ-60 improves liver fibrosis in mice with non-alcoholic fatty liver disease by inhibiting the SP1/TGF-β/Smad3 signaling axis].
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Geng Zhaodie, Hu Li, Dai Yunli, Luo Ronggang, Xu Tao, Liao Xuyang, Yuan Zhiping, Wang Jianta, Xiao Ying
Аннотация
OBJECTIVES: To investigate the mechanism of XJ-60, a derivative of cajanonic acid A, for alleviating liver fibrosis in mice with non-alcoholic fatty liver disease (NAFLD).
METHODS: Twelve db/db mice were randomized equally into NAFLD model group and XJ-60 treatment group with daily gavage of 50 mg/kg XJ-60, with 6 db/m mice serving as the control group. Successful modeling of NAFLD was validated using HE and Oil Red O staining and by measuring ALT and AST levels of the mice. Immunohistochemistry was used for detecting hepatic expressions of specific protein 1 (SP1) and fibronectin (FN); the changes in hepatic expressions of epithelial-mesenchymal transition (EMT) markers, extracellular matrix (ECM) markers, and IL-6 were detected using Western blotting and ELISA. In AML12 cells induced with free fatty acids (FFA), the effect of XJ-60 on expressions of SP1, transforming growth factor-β (TGF-β), Smad3/p-Smad3, and the markers of EMT and ECM were analyzed. SP1 knockdown experiment was performed to validate the role of TGF‑β/Smad3 signaling axis in NAFLD.
RESULTS: XJ-60 treatment significantly reduced serum lipid levels, improved liver histology, and lowered hepatic IL-6 expression in db/db mice. The expression level of SP1 was positively correlated with α-SMA and negatively with E-ca expression. In AML12 cells, XJ-60 treatment at 10 μmol/L significantly reduced FFA-induced lipid accumulation and downregulated cellular expressions of SP1, TGF-β, p-Smad3, and the EMT and ECM markers; SP1 knockdown obviously inhibited the expression levels of TGF-β, Smad3 and ECM markers.
CONCLUSIONS: XJ-60 ameliorates liver fibrosis and steatosis in mice with NAFLD possibly through SP1-mediated inhibition of the TGF‑β/Smad3 pathway to reduce ECM deposition.
METHODS: Twelve db/db mice were randomized equally into NAFLD model group and XJ-60 treatment group with daily gavage of 50 mg/kg XJ-60, with 6 db/m mice serving as the control group. Successful modeling of NAFLD was validated using HE and Oil Red O staining and by measuring ALT and AST levels of the mice. Immunohistochemistry was used for detecting hepatic expressions of specific protein 1 (SP1) and fibronectin (FN); the changes in hepatic expressions of epithelial-mesenchymal transition (EMT) markers, extracellular matrix (ECM) markers, and IL-6 were detected using Western blotting and ELISA. In AML12 cells induced with free fatty acids (FFA), the effect of XJ-60 on expressions of SP1, transforming growth factor-β (TGF-β), Smad3/p-Smad3, and the markers of EMT and ECM were analyzed. SP1 knockdown experiment was performed to validate the role of TGF‑β/Smad3 signaling axis in NAFLD.
RESULTS: XJ-60 treatment significantly reduced serum lipid levels, improved liver histology, and lowered hepatic IL-6 expression in db/db mice. The expression level of SP1 was positively correlated with α-SMA and negatively with E-ca expression. In AML12 cells, XJ-60 treatment at 10 μmol/L significantly reduced FFA-induced lipid accumulation and downregulated cellular expressions of SP1, TGF-β, p-Smad3, and the EMT and ECM markers; SP1 knockdown obviously inhibited the expression levels of TGF-β, Smad3 and ECM markers.
CONCLUSIONS: XJ-60 ameliorates liver fibrosis and steatosis in mice with NAFLD possibly through SP1-mediated inhibition of the TGF‑β/Smad3 pathway to reduce ECM deposition.