Fig 1: CVF pretreatment preserves integrity of tight junctions and blood-air barrier in IR condition. (A) Representative Western blot images of ICAM1 in lung tissues (The grouping of gels/blots cropped from different parts of the same gel). (B) Graphic presentation of ICAM1 abundance in lung tissues. (C) Representative Western blot images of ZO-1 in lung tissues (The grouping of gels/blots cropped from different parts of the same gel). (D) Graphic presentation of ZO-1 abundance in lung tissues. (E) Representative Western blot images of MMP2 in lung tissues (The grouping of gels/blots cropped from different parts of the same gel). (F) Graphic presentation of MMP2 abundance in lung tissues. (G) Representative Western blot images of MMP9 in lung tissues (The grouping of gels/blots cropped from different parts of the same gel). (H) Graphic presentation of MMP9 abundance in lung tissues. (*P < 0.05, compared with control. #P < 0.05, compared between I/R and I/R + CVF group).
Fig 2: Effect of XDT on the level of TNF-α, IL-1β, NF-κb, ICAM-1, MMP-9, ET-1, NO, SOD, and TXB2 on yeast-induced fever in rats by ELISA. Data are expressed as the mean ± SD. ∗∗∗P < 0.001 vs. the control group; #P < 0.05, ##P < 0.01, and###P < 0.001 vs. the model group; &P < 0.05 vs. the XDT 2.70 group; ¥P < 0.05 vs. the XDT 0.68 group; n = 8.
Fig 3: Effect of DGLL on the expression of inflammatory cytokines and adhesion molecules induced by LPS. Expression levels of (A) TNF-a and (B) IL-1ß in rat lung tissue as detected by ELISA. (C) Representative western blotting image and corresponding quantification analysis of ICAM-1 expression levels in rat lung tissue. Quantification of the levels of (D) TNF-a and (E) IL-1ß in RAW264.7 cell culture supernatant after LPS with/without DGLL treatment as detected by ELISA. (F) Representative western blotting image and corresponding quantification analysis of ICAM-1 expression in RAW264.7 cells. All data are expressed as the mean ± SEM. *P<0.05 vs. Sham; #P<0.05 vs. LPS. DGLL, diammonium glycyrrhizinate lipid ligand; IL, interleukin; LPS, lipopolysaccharide; ICAM-1, intercellular adhesion molecule-1; TNF, tumor necrosis factor.
Fig 4: Effect of XDT-cs on the protein level of ICAM-1, MMP-9, COX-2, and p65 in glutamate-induced PC12 by WB assay. Representative bands are shown in (a). The levels of ICAM-1 (b) and MMP-9 (c), and COX-2 (d) and phosphorylation levels of p65 (e) were normalized to the control. Results were expressed as the mean ± SD (n = 3). **P < 0.01 vs. the control group; #P < 0.05 and ##P < 0.01 vs. the model group.
Fig 5: HMGB1‐TLR4 signalling pathway mediates the migration, adhesion and activation of dendritic cells (DCs) in ischaemia‐reperfusion myocardium. A, Double immunofluorescence of DCs in myocardial tissue among all groups (n = 10 for each group). Samples were collected right after IR procedure and staining was performed as described in Section 2. Representative fluorescence images (200×) of the distribution of CD1a (green), of CD80 (red). Arrows indicate co‐localization. (B,C) The geometric mean optical density of CD80, CD86 among all groups (n = 10 for each group) in peripheral blood of rats was detected by flow cytometry. Histological study, immunohistochemical staining in cardiac tissues from rats of different groups (n = 10 for each group). Samples were collected right after IR procedure was over and staining. D, Hematoxylin‐eosin (HE) staining pictures (200×) are shown in the left, immunohistochemical staining pictures (200×) are in the middle and right; (E) integral optical density (IOD) of ICAM‐1; (F) IOD of E‐selectin; (G) IOD of P‐selectin. Scale bars, 100 μm. *P < 0.05, comparisons of IR‐C, IR‐H‐Ig and IR‐Ig groups with Sham group; #P < 0.05, comparisons of IR‐H‐Ig and IR‐Ig group with IR‐C group
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