Additional file 1 of NecroX-5 ameliorates bleomycin-induced pulmonary fibrosis via inhibiting NLRP3-mediated epithelial–mesenchymal transition

Autor: Min, Li, Shu-Li, Zhang, Feng, Yuan, Han, Hu, Shao-Jun, Li, Sheng-Xiong, Tong, Jia-Yu, Tian, Xiang-Zhi, Fang, Dan, Feng
Rok vydání: 2022
Předmět:
DOI: 10.6084/m9.figshare.19808072
Popis: Additional file 1: Fig S1. NecroX-5 ameliorated pulmonary damage in BLM-treated mice. (A) Design of animal experiments. (B). HE staining. (C). Lung injury score. (D). The levels of TNF-α in BALF. (E). The levels of IL-1β in BALF. (F) neutrophil number in BALF. (G) Lung tissue levels of MPO. (H) Lung tissue levels of SOD. (I) Mitochondrial MDA levels in lung tissue. (J) Cytosolic MDA levels in lung tissue. *P < 0.05vs. control; &P < 0.05 vs. BLM. Fig S2. NecroX-5 inhibited inflammation and oxidative stress in pulmonary epithelial cells exposed BLM. (A) The levels of TNF-α in MLE-12 cells. (B) The levels of IL-1β in MLE-12 cells. (C) The levels of TNF-α in BEAS-2B cells. (D) The levels of IL-1β in BEAS-2B cells. (E) The levels of intracellular ROS. Bar=10um. (F) The levels of mitochondrial ROS. Bar=10um. (G)mitochondrial morphology by TEM. Bar=1um. *P < 0.05 vs. control; &P < 0.05 vs. BLM. Fig S3. The upregulation of NLRP3 was confirmed by western blotting. (A) The expression of NLRP3 in MLE-12 cells. (B) The expression of NLRP3 in MLE-12 cells. Fig S4. NLRP3 overexpression eliminated the inhibitory effect of NecroX-5 on inflammation and oxidative stress. (A) The levels of TNF-α in MLE-12 cells. (B) The levels of IL-1β in MLE-12 cells. (C) The levels of TNF-α in BEAS-2B cells. (D) The levels of IL-1β in BEAS-2B cells. (E) The levels of intracellular ROS. Bar=10um. *P < 0.05 vs. OE-NC. Table S1. Human primers used and RT-PCR conditions. Table S2. Mouse primers used and RT-PCR conditions. Table S3. Antibodies used for Western blot, and immunofluorescence.
Databáze: OpenAIRE