Abstract

Abstract Objectives To establish model mice with acute pancreatitis (AP) and study influence of calcitonin gene-related peptide (CGRP) on AP. Methods The model mice with AP were firstly established by intraperitoneal injection of successive six doses of caerulein (100 μg/kg) and one dose of lipopolysaccharide (10 mg/kg). The intraperitoneal injection of CGRP (100 μg/kg) was performed to investigate influence of CGRP on AP, mainly involving the determination of amylase activity and the expression of CGRP and CD20+ B lymphocytes. Results CGRP on mice with AP could significantly reduce the severity of pancreatic pathological injury, the activity of amylase and the expression of CD20+ B lymphocytes. CGRP was significantly expressed in pancreatic tissue with AP, but CGRP receptor antagonist down-regulated the expression of CGRP and increased the number of CD20+ B lymphocytes, confirming the protective effect of CGRP on pancreatic tissue. Conclusions We preliminarily conclude that CGRP could significantly improve the pancreatic lesions and inflammatory infiltration of pancreas in mice with AP, and reduce the damage of pancreatic acinar cells, by mainly increasing blood flow and blood flow velocity of pancreas to improve the pancreatic microcirculation and effectively reducing the permeability of the microvessels to decrease the pathological damage degree of AP.

Highlights

  • Pancreas lying in the upper abdomen behind the stomach is an exocrine organ that makes and secretes digestive enzymes into the intestine, and an endocrine organ that makes and secretes hormones into the blood to control energy metabolism and storage throughout the body [1]

  • We preliminarily conclude that calcitonin gene-related peptide (CGRP) could significantly improve the pancreatic lesions and inflammatory infiltration of pancreas in mice with acute pancreatitis (AP), and reduce the damage of pancreatic acinar cells, by mainly increasing blood flow and blood flow velocity of pancreas to improve

  • There was a small amount of fluid in the abdominal cavity of mice with AP, obvious saponification spots occurred in the mesentery and omentum, and the pancreas had a severe adhesion to the surrounding tissues

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Summary

Introduction

Pancreas lying in the upper abdomen behind the stomach is an exocrine organ that makes and secretes digestive enzymes into the intestine, and an endocrine organ that makes and secretes hormones into the blood to control energy metabolism and storage throughout the body [1]. Acute pancreatitis (AP) can cause the pancreas itself to be digested, and it is believed that the premature activation of digestive enzymes, especially trypsin, leads to the digestion of the pancreas and causes acute inflammation of pancreas [2]. Intra-acinar trypsin activation was considered the key event in acute pancreatitis, and this trypsin centric hypothesis was supported by various observations [2]. Ninety percent of pancreas is composed of acinar cells which secrete digestive enzymes such as trypsin, chymotrypsin, and amylase for digestion of food in the small intestine [3]. Pancreatic exocrine secretion is regulated by a variety of neurotransmitters, including acetylcholine, vasoactive intestinal peptide, gastrin releasing peptide, neuromedin C, neurotensin, substance P, calcitonin gene-related peptide, etc. Pancreatic exocrine secretion is regulated by a variety of neurotransmitters, including acetylcholine, vasoactive intestinal peptide, gastrin releasing peptide, neuromedin C, neurotensin, substance P, calcitonin gene-related peptide, etc. [3]

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