首页|铁死亡对急性胰腺炎胰腺组织炎症损伤影响的初探

铁死亡对急性胰腺炎胰腺组织炎症损伤影响的初探

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目的 观察急性胰腺炎(acute pancreatitis,AP)中是否存在铁死亡以及铁离子对核苷酸结合寡聚化结构域受体蛋白3(NLRP3)途径的影响,探讨保护胰腺腺泡细胞的机制.方法 将45只雄性C57BL/6小鼠随机分为3组[对照组、AP 组、AP+2'2-联吡啶组(2'2-bipyridyl)].50μg/kg 的雨蛙素(caerulein)共注射 12 次,每次间隔 1 h.AP+2'2-bipyridyl组在注射caerulein之前用2'2-bipyridyl(20 mg/kg)预处理1 h.对照组则注射等量的正常生理盐水.所有的小鼠在最后一次注射后1 h被处死.收获的胰腺用于组织病理学评估、免疫组织化学分析、试剂盒检测和Western blotting检测.结果 铁死亡抑制剂2'2-bipyridyl可以防止铁离子的积累,减少脂质过氧化物的形成;它还可以通过NLRP3途径减轻胰腺炎症损伤.结论 铁死亡这种细胞死亡方式在AP中真实存在,抑制铁死亡可以减轻AP时的胰腺炎症损伤.
The effect of ferroptosis on pancreatic inflammatory injury in acute pancreatitis
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.

acute pancreatitis(AP)ferroptosislipid peroxidationinflammasomecytokine

李杰、冯语森、黄子键、王刚

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哈尔滨医科大学附属第一医院胰胆外科肝脾外科教育部重点实验室,黑龙江哈尔滨 150001

急性胰腺炎(AP) 铁死亡 脂质过氧化物 炎症小体 细胞因子

国家自然科学基金国家自然科学基金

8207065782370651

2024

西安交通大学学报(医学版)
西安交通大学

西安交通大学学报(医学版)

CSTPCD北大核心
影响因子:1.144
ISSN:1671-8259
年,卷(期):2024.45(2)
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