Figure 3
From: S-maltoheptaose targets syndecan-bound effectors to reduce smoking-related neutrophilic inflammation
Dose-dependent decrease in unopposed NE with airway treatment of S-maltoheptaose.
(A) Airway treatment of cigarette smoke-exposed rats (CS, n = 8) with S-maltoheptaose-on-chitosan carrier beads resulted in dose-dependent decrease in unopposed NE despite negligible change in total NE in BALF samples. NE levels of the sham air controls (SA, n = 8) are included for comparison. **P < 0.001, *P < 0.01. (B) Western blots of the BALF samples were performed for NE (a), syndecan-1 (SDC-1), (b) and α1-AT (c); casein zymography of the BALF samples was performed in parallel (d). NE and α1-AT remained co-localized with SDC-1 in the nominal range of 90–250 kD (Lanes 1 and 2 of each panel); this range indicated proteolytic activity (panel d, Lane 1) that was inhibited by treatment with Eglin C tetrapeptide (Panel d, Lane 2). In BALF samples of rats given airway treatment of S-maltoheptaose, NE- and α1-AT-immunopositivites extended beyond the SDC-positive region (Panels a–c, Lanes 3–5) in correlation with no proteolytic activity in the casein zymogram (Panel d, Lanes 3–5). When NE was displaced from SDC-1, it became accessible to inhibition by α1-AT. Lanes 1: neat BALF; Lanes 2: Eglin c-treated BALF; Lanes 3–5: BALF from smoke-exposed rats treated respectively with 20 μg, 100 μg and 500 μg of S-maltoheptaose on carrier beads via the airways.
