Nikotinin Sıçan Pankreatit Modelindeki Hafifletici Etkisinde Vagusun Rolünün Araştırılması

Authors : Meltem Kolgazi, Zozan Güleken, Bircan Kolbaşi, Canberk Sami Başibüyük, Feriha Ercan, Berrak Yeğen

Pages : 166-175

Doi:10.31067/acusaglik.849995

View : 31 | Download : 8

Publication Date : 2021-04-01

Article Type : Research

Abstract :The anti-inflammatory effects of nicotine on various organs and the involvement of the cholinergic anti-inflammatory pathway activation in these effects were previously shown. The purpose of the study is to evaluate the effects of nicotine treatment on acute pancreatitis model and to investigate the association of cholinergic pathway with these effects.In Wistar albino rats common pancreatic-biliaryduct was ligated (PBDL) or sham-operation were performed. In PBDL rats, vagal afferent denervation (perivagal capsaicin; 10mg/ml) or truncal vagotomy was appliedor the vagi were left intact. Postoperatively, PBDL groups were treated intraperitoneally with either nicotine (1 mg/kg/day) or saline for 4 days. Following decapitation on the 4th day, serum tumor necrosis factor (TNF)-and interleukin (IL)-10 levels andmyeloperoxidase activity (MPO), malondialdehiyde (MDA) and glutathione (GSH) levels in the pancreas, liver and lung tissues were measured, and histopathological analyses were made. While the TNF-α level was significantly higher in the PBDL group than in the YC group, it was significantly lower in the subjects takennicotine treatment. IL-10 level was lower in the PBDL group treated with saline than in the YC group and an increase was observed with nicotine treatment.Compared to sham-operated group, microscopic damage scores, MDA, MPO levels in the pancreas, liver and lung tissues of the PBDL group were elevated, while GSH levels were reduced. Nicotine treatment depressed MDA and MPO levels,preserved GSH contents and reduced histological damage in the pancreas and liver. Vagal afferent denervation or truncal vagotomy did not alter these protective effects of nicotine. The results suggest that the protective effects of nicotine on pancreatic inflammation could occur independently of the vagal pathways, but directly by the activation of 7nAChR on the immune cells and by inhibiting neutrophil infiltration and pro-inflammatory cytokine release.
Keywords : pancreatitis, nicotine, vagus, inflammation, pancreatic duct ligation