Introduction: Acute pancreatitis is an inflammatory condition that may lead to multisystemic organ failure. The "cholinergic anti-inflammatory pathway" modulates the immune system by acting via the alpha7 receptors expressed on macrophages and immune cells.
Aim: The aim of this study was to investigate the effects of cholinergic anti-inflammatory pathway on acute pancreatitis induced by pancreaticobiliary obstruction in rats.
Materials and Methods: Acute pancreatitis was induced in Wistar albino rats by pancreaticobiliary duct ligation (PBDL). Half of the animals, before they were induced with pancreatitis, were subjected to bilateral cervical vagotomy using capsaicin. All groups were treated intraperitoneally with either nicotine (1 mg/kg/day) or saline for 3 days. After decapitation, lung, liver and pancreas tissues were collected for histologic evaluation and measurement of myeloperoxidase (MPO) activity, malondialdehyde (MDA) and glutathione (GSH) levels. For lung tissue (1) vascular congestion, (2) fibrosis and interstitial edema, (3) alveolar structural disturbance and inflammatory cell infiltration, for pancreas tissue (1) edema, (2) acinar necrosis and (3) inflammatory cell infiltration, for liver tissue (1) vacuolization and picnotic nucleus in hepatocytes, (2) sinusoidal congestion and (3) Kupffer cell infiltration were taken as the scoring criteria. Based on a semiquantitative scale, the histological scores of the organs were calculated as the sum of the scores (0–3) given for each criterion. The maximum calculated score was 9. Student’s t-test was used for statistical analysis. Values of p<0.05 were regarded as significant.
Results: Acute pancreatitis with PBDL increased microscopic damage scores in lung, liver and pancreas tissues. Nicotine treatment and cervical vagotomy significantly reduced microscopic damage scores compared with PBDL group in all tissues (p<0.05-0.001). Nicotine treatment reduced MPO activity and MDA levels which were increased with PBDL in all three tissues, and prevented PBDL-induced GSH depletion in the liver and pancreas tissues (p<0.05-0.001). Similarly, capsaicin-induced denervation decreased MPO activity and MDA levels in liver and pancreas tissues (p<0.05-0.001).
Conclusion: Stimulation of the cholinergic system with nicotine reduced neutrophil infiltration and lipid peroxidation and prevented GSH depletion in the PBDL-induced acute pancreatitis model. In addition, capsaicin-sensitive vagal afferent neurons have a role in this cholinergic anti-inflammatory mechanism. Further experimental and clinical studies are required to elucidate the regulatory role of the cholinergic system in acute pancreatitis.