Fig. 4

Overexpression of ACSM5 inhibited FFA-induced lipid accumulation and fibrosis in LF cells by regulating the FABP4-mediated PPARγ signaling. (A) LF cells infected with ADV-ACSM5 alone or in combination with ADV-FABP4 were treated with FFA for 48 h, and the protein expression of ACSM5, FABP4 and PPARγ in LF cells was detected by western blot. (B and C) LF cells infected with ADV-ACSM5 alone or in combination with ADV-FABP4 were treated with FFA for 48 h, and oil red O staining was used to detect intracellular lipid accumulation in LF cells. Bar size = 100 nm. (D) LF cells infected with ADV-ACSM5 alone or in combination with ADV-FABP4 were treated with FFA for 48 h, and TG assay kit was used to detect TG levels in LF cells. (E and F) LF cells infected with ADV-ACSM5 alone or in combination with ADV-FABP4 were treated with FFA for 48 h, and the protein expression of FASN and ACC in LF cells was detected by western blot. (E and H) LF cells infected with ADV-ACSM5 alone or in combination with ADV-FABP4 were treated with FFA for 48 h, and the protein expression of collagen I, collagen III and α-SMA in LF cells was detected by western blot. LF, ligamentum flavum. FFA, free fatty acids. ADV, adenovirus. NC, negative control. ^n.s.P > 0.05, ^#P < 0.05, ^##P < 0.01, and ^###P < 0.001