Fig 2: The silencing of SAAL1 alleviated LPS-induced inflammation and suppressed the NLR signaling pathway. The production of TNF-a (A), IL-6 (B), and IL-1ß (C) in the A549 cells was measured by ELISAs. (D) The protein levels of NLRP3, NOD1, and MAPK1 in the A549 cells was checked by western blotting. **, P<0.01 vs. control group; ##, P<0.01 vs. si-NC + LPS group. SAAL1, serum amyloid A-like 1; LPS, lipopolysaccharide; TNF-a, tumor necrosis factor alpha; IL-1ß, interleukin-1 beta; ELISAs, enzyme-linked immunosorbent assays; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; si-NC, small interfering RNA negative control.

Fig 3: The silencing of SAAL1 ameliorated LPS-induced lung injury and inflammation. (A) The messenger RNA level of SAAL1 in the lung tissues was checked by qRT-PCR. (B) H&E staining was used to check lung tissue injury (magnification 400×). (C) The W/D weight ratio of the lung tissues, (D) neutrophil number, and (E) MPO activity was determined. (F-H) The production of TNF-a (F), IL-6 (G), and IL-1ß (H) in the lung tissues was measured by ELISAs. (I) The protein levels of SAAL1, TNF-a, IL-6, and IL-1ß in the lung tissues was measured by western blotting. **, P<0.01 vs. control group; ##, P<0.01 vs. shNC + LPS group. SAAL1, serum amyloid A-like 1; LPS, lipopolysaccharide; qRT-PCR, quantitative real-time polymerase chain reaction; H&E, hematoxylin and eosin; W/D, wet/dry; MPO, myeloperoxidase; TNF-a, tumor necrosis factor alpha; IL-1ß, interleukin-1 beta; ELISAs, enzyme-linked immunosorbent assays; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; shNC, short hairpin RNA negative control.

Fig 4: The silencing of SAAL1 alleviated the LPS-induced cell apoptosis by modulating the NLR signaling pathway. (A) The expression of NLRP3 protein in the A549 cells was measured by western blotting. (B) Cell viability was checked by CCK-8. (C) Cell apoptosis was detected by flow cytometry. (D-F) The production of TNF-a, IL-6, and IL-1ß in the A549 cells was measured by ELISAs. **, P<0.01 vs. si-NC + LPS group; ##, P<0.01 vs. si-SAAL1 + Vector + LPS group. SAAL1, serum amyloid A-like 1; LPS, lipopolysaccharide; CCK-8, Cell Counting Kit-8; TNF-a, tumor necrosis factor alpha; IL-1ß, interleukin-1 beta; ELISAs, enzyme-linked immunosorbent assays; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; si-NC, small interfering RNA negative control.

Fig 5: The silencing of SAAL1 alleviated LPS-induced cell apoptosis in vitro. (A) The protein levels of SAAL1 in the A549 cells stimulated with LPS was checked by western blotting assays. (B) The protein level of SAAL1 in the A549 cells was checked by western blotting assays. (C) The cell viability was checked by CCK-8 assays. (D) The cell apoptosis was detected by flow cytometry. (E) The protein levels of Ki67, Bcl-2, caspase-1, and Bax in the A549 cells were detected by western blotting assays. **, P<0.01 vs. control group; ##, P<0.01 vs. si-NC + LPS group. SAAL1, serum amyloid A-like 1; LPS, lipopolysaccharide; CCK-8, Cell Counting Kit-8; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; si-NC, small interfering RNA negative control.