- VernacularTitle:铁死亡对急性胰腺炎胰腺组织炎症损伤影响的初探
- Author:
Jie LI
1
;
Yusen FENG
1
;
Zijian HUANG
1
;
Gang WANG
1
Author Information
- Publication Type:Journal Article
- Keywords: acute pancreatitis (AP); ferroptosis; lipid peroxidation; inflammasome; cytokine
- From: Journal of Xi'an Jiaotong University(Medical Sciences) 2024;45(2):178-182
- CountryChina
- Language:Chinese
- Abstract: 【Objective】 To observe the presence of ferroptosis in acute pancreatitis (AP) and the effect of iron ions on the NLRP3 pathway so as to explore the possible mechanisms for the protection of pancreatic alveolar cells. 【Methods】 A total of 45 male C57BL/6 mice were randomly divided into three groups (control, AP, and AP+2′2-bipyridyl). A total of 12 injections (caerulein, 50 μg/kg) were given at one-hour intervals. The AP+2′2-bipyridyl group was pretreated with 2′2-bipyridyl (20 mg/kg) for 1 hour, and then injected with caerulein. The control group was injected with an equal volume of normal saline. All of the mice were killed one hour after the last injection. Their pancreases were harvested for histopathological evaluation, immunohistochemistry analyses, and Western blotting. 【Results】 The ferroptosis inhibitor 2′2-bipyridyl could prevent the accumulation of iron ions, reduce the formation of lipid peroxides and the injury in the process of AP, and it also reduced pancreatic inflammation through NLRP3 pathway. 【Conclusion】 This experiment confirmed the real existence of ferroptosis, a form of cell death, in AP, and revealed that inhibition of ferroptosis can reduce pancreatic inflammatory damage in AP.