Effect of cholecystokinin octapeptide on tumor necrosis factor α transcription and nuclear factor-κB activity induced by lipopolysaccharide in rat pulmonary interstitial macrophages

Figure 2 sCCK-8 inhibited LPS-induced NF-κB binding in PIMs in a dose-dependent manner through CCK receptor. A: Representative autoradiography picture of three experiments of EMSA. Lane 1, negative control; lane 2, positive control; lane 3, ³²P-labeled NF-κB Oligo plus unlabeled NF-κB Oligo (competitor); lane 4, ³²P-labeled NF-κB Oligo plus unlabeled AP-2 Oligo (noncompetitor); lane 5, control; lane 6, LPS; lane 7, LPS + CCK 10^-8 mol·L^-1; lane 8, LPS + CCK 10^-7 mol·L^-1; lane 9, LPS + CCK 10^-6 mol·L^-1; lane 10, LPS + CCK + proglumide; lane 11, CCK 10^-7 mol·L^-1. B: Densitometry of EMSA showing decreased NF-κB binding in PIMs treated with sCCK-8. n = 3, ¯x ± s, ^aP > 0.05, ^cP < 0.01 vs control; ^eP < 0.05, ^fP < 0.01 vs LPS; ⁱP < 0.01 vs LPS + CCK 10^-7 mol·L^-1.