Basic Study
Copyright ©The Author(s) 2021.
World J Biol Chem. Jan 27, 2021; 12(1): 1-14
Published online Jan 27, 2021. doi: 10.4331/wjbc.v12.i1.1
Figure 3
Figure 3 Cyclic adenosine monophosphate inhibits lipopolysaccharide-induced matrix-metalloproteinase-9 and tumor necrosis factor α secretion. A: SDS-PAGE/immunoblot of cell supernatants. Lane 1 is a matrix-metalloproteinase-9 (MMP-9) standard; B: Densitometry of Panel A. Each data bar is the average ± standard error for three independent densitometry measurements; and C: Tumor necrosis factor α (TNFα) levels were determined in cell supernatants by enzyme-linked immuno sorbent assay and each data bar is the average ± standard error for three independent measurements. THP-1 monocytes were treated with 3',5'-cyclic adenosine monophosphate (300 μmol/L) followed by lipopolysaccharide (0.03 μg/mL) for 6, 48, and 72 h. Cells were collected, centrifuged at 500 g for 10 min and supernatant assessed for (A) MMP-9 and (C) TNFα. Statistical differences (aP < 0.05 or bP < 0.01) between MMP-9 secretion at different lipopolysaccharide treatment times and 3',5'-cyclic adenosine monophosphate inhibition of either MMP-9 or TNFα secretion are shown. LPS: Lipopolysaccharide; MMP-9: Matrix-metalloproteinase-9; TNFα: Tumor necrosis factor α; Bt2-cAMP: 3',5'-cyclic adenosine monophosphate.