Fig 1: Effects of ECM components on the downstream molecules in ASMCs. Relative expression of TGFß1, FGF-1, MMP-9 and TIMP1 was determined in ASMCs following treatment with ECM components, including COL-1, LN and COL-3 by (A) reverse transcription-quantitative polymerase chain reaction and (B) western blotting. Data are presented as the mean ± standard deviation in triplicate. *P<0.05 and **P<0.01 vs. the control group. ECM, extracellular matrix; ASMCs, airway smooth muscle cells; COL, collagen; LN, laminin; TGFß1, transforming growth factor ß-1; FGF-1, fibroblast growth factor-1; MMP-9, matrix metalloproteinase-9; TIMP1, metalloproteinase inhibitor 1; COPD, chronic obstructive pulmonary disease.
Fig 2: Effects of ECM components on cytokines in ASMCs. The expression of MMP-9, CXCL1, CXCL8 and IL-6 was determined following treatment with ECM components, including COL-1, LN and COL-3 in (A) normal ASMCs and (B) ASMCs from rat model of chronic obstructive pulmonary disease using ELISA assay. Data are presented as the mean ± standard deviation in triplicate. *P<0.05, **P<0.01 and ***P<0.001 vs. the control group. ECM, extracellular matrix; ASMCs, airway smooth muscle cells; MMP-9, matrix metalloproteinase-9; COL, collagen; LN, laminin; CXCL, C-X-C motif chemokine ligand; IL-6, interleukin-6.
Fig 3: SIS3 inhibits mRNA expression of RAGE, TGF-ß1, MMP2, and MMP9 in lung homogenates of ARDS rats. The mRNA levels of RAGE, TGF-ß1, MMP2, and MMP9 were determined using real-time PCR and were standardized to ß-actin. The results suggested that SIS3 inhibited the increase of (a) RAGE, (b) TGF-ß1, (c) MMP2, and (d) MMP9 in LPS-induced lung homogenates of ARDS rats, while no effect was seen upon pretreatment with PBS. The data are presented as the means ± SD (n = 10). ?P < 0.05 vs. CTL; #P < 0.05 vs. ARDS.
Fig 4: MMP-2, MMP-9 and TIMP-1 levels in lung tissues of rats exposed to BPA/H2S. The results are presented as the mean ± SE (n = 8 rats). a) Significant difference versus control group at P = 0.05. b) Significant difference versus BPA group at P = 0.05
Fig 5: SIS3 pretreatment prevented the reduction of the expression of RAGE, TGF-ß1, MMP2, and MMP9 in LPS-induced ARDS. The effects of SIS3 on the protein expression levels of (a) RAGE, (b) TGF-ß1, (c) MMP2, and (d) MMP9 in the BALF and sera of the ARDS rats were determined using ELISA. The results demonstrated that the levels of RAGE, TGF-ß1, MMP2, and MMP9 proteins were significantly higher in the ARDS group than in the control group, while the levels of RAGE, TGF-ß1, MMP2, and MMP9 in the SIS3 group were lower than those in the ARDS group. The protein levels of RAGE, TGF-ß1, MMP2, and MMP9 in LPS-administered pretreatment with PBS were not different from those of the ARDS group. The data are presented as the means ± SD of three independent experiments in triplicate (n = 10). ?P < 0.05 vs. CTL; #P < 0.05 vs. ARDS.
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