Research Paper Volume 13, Issue 10 pp 13807—13821
Acetyl oxygen benzoate engeletin ester promotes KLF4 degradation leading to the attenuation of pulmonary fibrosis via inhibiting TGFβ1–smad/p38MAPK–lnc865/lnc556–miR-29b-2-5p–STAT3 signal pathway
Figure 5. AOBEE attenuated pulmonary fibrosis by blocking the lnc865/lnc556–miR-29b-2-5p–STAT3 axis. (A) RNA-FISH showed that lnc865 and lnc556 mainly existed in the cytoplasm, and AOBEE induced a decrease of their expression but did not cause their translocation. (B) The rescue experiments reflected that si-lnc865 and si-lnc556 decreased lnc865 and lnc556 expression, but the miR-29b-2-5p inhibitor increased their expression. (C) The rescue experiments showed that si-lnc865 and si-lnc556 induced a substantial decrease of vimentin, α-SMA, and collagen I and III, but the miR-29b-2-5p inhibitor induced a substantial increase of the expression of these proteins. (D) RNA interference on lnc865 and lnc556 increased miR-29b-2-5p expression. (E) AOBEE promoted miR-29b-2-5p expression. (F) Western blot revealed that si-lnc865 and si-lnc556 decreased STAT3 and p-STAT3 expression. (G) The rescue experiments demonstrated that the miR-29b-2-5p inhibitor reversed the effects of si-lnc865 and si-lnc556. Each bar represents the mean ± SD, n = 6; *p < 0.05, **p < 0.01.