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. 2016 Apr 22;13(6):5005–5012. doi: 10.3892/mmr.2016.5168

Figure 3.

Figure 3

Increased severity of inflammatory reaction is mediated by NF-κB and TNF-α. (A–C) The immunostaining of NF-κB subunit P65 is demonstrated in the control, scramble and V1-siRNA groups (magnification, ×200; scale bar in vignettes=20 mm). P65 remained stable prior to LPS administration. (D–F) The immunostaining of P65 was demonstrated in the LPS, scramble+LPS and V1-siRNA+LPS groups (magnification, ×200; scale bar in vignette=20 mm). P65 was phosphorylated following LPS insult, immunostaining was more marked in the (F) V1-siRNA+LPS group, compared with the (D) LPS and (E) scramble+LPS groups (red arrows show positive staining). (G) mRNA levels of TNF-α were increased in all ALI groups, but were higher in the V1-siRNA+LPS group. (H–J) ELISA indicated TNF-α as a mediator of the severe inflammatory reaction, as TNF-α was the only molecule to show a consistent increasing trend in the (H) tissue homogenates, (I) BALF and (J) plasma. TNF-α was higher in the V1-siRNA+LPS group in all samples, IL-6 increased without statistical significance. Data are presented as the mean ± standard deviation. *P<0.05, vs. control group; #P<0.01, vs. control group; %P<0.05, vs. LPS group; $P=0.01, vs. LPS group; &P<0.01, vs. LPS group. NF-κB, nuclear factor-κB; TNF-α, tumor necrosis factor-α, IL-6, interleukin-6; siRNA, small interfering RNA; ALI, acute lung injury; LPS, lipopolysaccharide; V1, versican V1; BALF, bronchoalveolar lavage fluid; ELISA, enzyme-linked immunosorbent assay.