Figure 4.

D₂ receptor signalling inhibits NF‐κB activation in AP. In vivo, AP was induced by injection of caerulein (100 μg·kg⁻¹) and LPS (5 mg·kg⁻¹) in Balb/C mice, and a D₂ agonist quinpirole (10 mg·kg⁻¹, i.p., 0.5 h before the first caerulein injection) was used instead of dopamine (50 mg·kg⁻¹, i.p., at the same time as caerulein). Mice were killed at 12 h after the first caerulein injection. In vitro, PACs were isolated from the pancreas of Balb/C mice. A D₂ agonist quinpirole (5 μM) was used instead of dopamine (500 μM) at the time of CCK (200 nM) stimulation. (A) Representative micrographs of H&E‐stained pancreatic sections (200×). (B) Histological score was determined as described in Methods. (C) Change in serum activity of amylase (left) and lipase (right). (D) Immunoblot analysis of IκBα, NF‐κBp65 phosphorylation levels and TNFα, IL‐1β and IL‐6 expression levels of pancreatic tissue in mice. (E) qRT‐PCR of mRNA levels of Tnfα, Il1β and Il6 in pancreatic tissue. (F) Immunoblot analysis of IκBα, NF‐κBp65 phosphorylation levels (at 1 h after CCK stimulation) and TNFα, IL‐1β and IL‐6 levels (at 4 h after CCK stimulation) in CCK‐stimulated PACs. (G) qRT‐PCR of mRNA levels of Tnfα, Il1β and Il6 in CCK‐stimulated PACs (at 4 h after CCK stimulation). (H) EMSA analysis of NF‐κB binding ability. n = 6 per group. Cae, caerulein; NC, normal control. Scale bar = 100 μm. *P < 0.05 versus NC; ^# P < 0.05 versus AP or CCK.