Vasorelaxing response to EGCG in the presence of selective COX-1 and COX-2 inhibitors in intact rat aortic rings.

<p>Increasing concentrations of EGCG were added to tissues pre-contracted with 10 µM NA and preincubated with L-NAME 100 µM alone or in the presence of either the selective COX-2 inhibitor SC236 10 nM or the selective COX-1 inhibitor SC560 10 nM. # <i>P</i><0.01 (EGCG+L-NAME) <i>vs</i> (EGCG); * <i>P</i><0.01 (EGCG+L-NAME+SC560) <i>vs</i> (EGCG+L-NAME).</p

Effect of DPI on EGCG-induced ROS production.

<p>HUVECs were pre-incubated with DPI 1 µM and treated with EGCG 100 µM for 30 min. Values are expressed as percentage ± SE (n = 3) of the amount of ROS generated under basal conditions. *<i>P</i><0.05 <i>vs</i> control and ^#<i>P</i><0.05 <i>vs</i> cells treated with EGCG.</p

Effect of treatment with selective COX-1 (SC560) or COX-2 (SC236) inhibitors toward PGI₂ production in HUVECs incubated with EGCG.

<p>Cells were incubated in medium 5% FCS in the presence of increasing concentrations of SC560 or SC236 (1–100 nM); 10 min after treatment with inhibitors, cells were added with arachidonic acid (10 µM) and EGCG (100 µM) for 30 min. PGI₂ was evaluated as 6-keto-PGF_1α in aliquots of cell supernatants using a specific EIA. Values are expressed as pg/ml ± SE (<i>n</i> = 3) of 6-keto-PGF_1α. # P<0.01 vs AA alone; *<i>P</i><0.05, **<i>P</i><0.01 <i>vs.</i> (AA+EGCG).</p

Effect of EGCG on intracellular ROS production.

<p>A) HUVECs were treated with EGCG (10, 50, 100 µM) for 30 minutes. B) HUVECs were treated with EGCG 100 µM for increasing times (15, 30, 60 min). Values are expressed as percentage ± SE (n = 14, A; n = 5, B) of the amount of ROS generated under basal conditions. *<i>P</i><0.05, **<i>P</i><0.1 <i>vs</i> control.</p

Effect of catalase on EGCG-induced ROS production.

<p>HUVECs were pre-incubated with catalase (300 U/ml) and treated with EGCG 100 µM for 30 min. Values are expressed as percentage ± SE (n = 3) of the amount of ROS generated under basal conditions. *<i>P</i><0.05 <i>vs</i> control and ^#<i>P</i><0.05 <i>vs</i> cells treated with EGCG.</p

PGI₂ production in perfusate from aortic rings treated with EGCG in the presence of selective COX-1 and COX-2 inhibitors.

<p>Samples from EGCG-treated aortic rings preincubated with L-NAME alone or in the presence of either the selective COX-2 inhibitor SC236 or the selective COX-1 inhibitor SC560 were collected and PGI₂ was evaluated as 6-keto-PGF_1α. Values are expressed as pg/ml of perfusate. °<i>P</i><0.01 <i>vs</i> L-NAME; *<i>P</i><0.01 <i>vs</i> (EGCG+L-NAME); #<i>P</i><0.01 <i>vs</i> (EGCG+L-NAME+SC560).</p

MOESM2 of Monitoring inflammation and airway remodeling by fluorescence molecular tomography in a chronic asthma model

Additional file 2: Figure S2 Representative images of histological slides obtained at 11 weeks from the lungs of mice receiving saline (Panel A) or DRA (Panel B) stained with Alcian/PAS, and from the lungs of mice receiving saline (Panel C) or DRA (Panel D) stained with Masson’s Trichrome. Alcian/PAS and Masson’s Trichrome staining were performed as described in "Methods"