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. 2022 Dec 17;8(12):e12385. doi: 10.1016/j.heliyon.2022.e12385

Figure 6.

Figure 6

LOX-1 silencing increased autophagy of HLSECs through AMPK/HNF4α signaling pathway. All groups were treated with 25 mM of glucose for 72 h, except for the normal control group. The cells in the transfection group HG + LV-LOX-1 or HG + LV-CON cells were blocked with AMPK (10 μM), HNF4α (0.6 μM), or autophagy (6 mM) inhibitors. The untreated intact samples were run as a control in each experiment. (A–C) HLSECs were cultured under the above conditions for 72 h, and the mRNA expression levels of LOX-1, Beclin-1, and LC3II in each group were determined by qRT-PCR. (D) The protein expression levels of each group were determined using western blotting, and β-actin was used as a loading control (see original blots in Supplemental Figure 6D). (E–K) Western blotting analyzed the relative protein expression of LOX-1, Beclin-1, LC3II, AMPK, p-AMPK, HNF4α, and p-HNF4α in each group (n = 3 independent experiments). All data are expressed as mean ± SD. from three independent experiments. ∗P < 0.05, ∗∗∗P < 0.01 versus the NC group; #P < 0.05, ###P < 0.001 versus HG + LV-CON group; xP < 0.05, xxP ​< 0.05, xxxP < 0.01 versus HG + LV-LOX-1 group.