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. 2022 Oct 27;15:3285–3301. doi: 10.2147/DMSO.S380053

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© 2022 Tong et al.

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FST knockdown aggravated lipid accumulation in LO2 cells and this effect was inhibited by rapamycin. (A and B) The efficiency of FST knockdown in LO2 cells was demonstrated by RT-qPCR and Western blotting. (C and D) Oil Red O staining and analysis results of FFA-treated negative control shRNA (NCsh) cells, FFA-treated FST-knockdown (FSTsh) cells, and FFA- and rapamycin-treated FSTsh (FSTsh+RAPA) cells (400×, scale bar: 50 µm). (E and F) The protein levels and analysis results of Akt, Akt-Thr308, Akt-Ser473, p-mTOR, and mTOR in FFA-treated NCsh cells and FFA-treated FSTsh cells. (G and H) The protein levels and analysis results of ACC1, FASN, SREBP1, ChREBP, and mTOR in NCsh, FSTsh, FSTsh+RAPA cells. β-actin was used as a loading control.

Notes: *P< 0.05, **P< 0.01, ***P< 0.001 vs NCsh group; ^#P< 0.05, ^##P< 0.01 vs FSTsh group.

Abbreviations: FST, follistatin; FFA, free fatty acid; SREBP1, sterol regulatory element-binding protein1; ChREBP, carbohydrate-responsive element-binding protein; ACC1, acetyl-CoA carboxylase1; FASN, fatty acid synthase; Akt, protein kinase B; mTOR, mammalian target of rapamycin; RAPA, rapamycin.