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大鼠巨噬细胞激活后胰腺腺泡细胞的不同细胞死亡模式

Different cell death modes of pancreatic acinar cells on macrophage activation in rats.

作者信息

Liang Tao, Liu Tie-fu, Xue Dong-bo, Sun Bei, Shi Li-jun

机构信息

Department of Digestive Diseases, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, China.

出版信息

Chin Med J (Engl). 2008 Oct 5;121(19):1920-4.

Abstract

BACKGROUND

The pathogenesis of acute pancreatitis is complex and largely unclear. The aim of this study was to explore the relationship between modes of cell death in pancreatic acinar cells, the release of cell contents and the inflammatory response of macrophages.

METHODS

Our experiment included four groups: group A (the control group), group B (AR42J cells overstimulated by caerulein), group C (AR42J cells treated with lipopolysaccharide and caerulein), and group D (AR42J cells treated with octreotide and caerulein). Apoptosis and oncosis, and the release of amylase and lactate dehydrogenase (LDH) from AR42J cells were detected. Rat macrophages were stimulated by 1 ml supernatant of culture medium of AR42J cells. Finally, NF-kappaB activation and TNF-alpha and IL-1beta secretion by macrophages were detected.

RESULTS

Oncotic cells in group C increased while apoptotic cells decreased (P < 0.05); cells in group D had the inverse reaction. The release of amylase and LDH changed directly with the occurrence of oncosis. The transcription factor NF-kappaB was activated and secretion of TNF-alpha and IL-1beta were significantly higher in group C than in group B (P < 0.05); in group D, these actions were significantly lower than in group B (P < 0.05). This trend was in line with changes in amylase and LDH production.

CONCLUSION

There is a close relationship between modes of pancreatic acinar cell death, the release of cell contents and the inflammatory reaction of macrophages.

摘要

背景

急性胰腺炎的发病机制复杂,在很大程度上尚不清楚。本研究的目的是探讨胰腺腺泡细胞的细胞死亡模式、细胞内容物释放与巨噬细胞炎症反应之间的关系。

方法

我们的实验包括四组:A组(对照组)、B组(用蛙皮素过度刺激的AR42J细胞)、C组(用脂多糖和蛙皮素处理的AR42J细胞)和D组(用奥曲肽和蛙皮素处理的AR42J细胞)。检测AR42J细胞的凋亡和胀亡,以及淀粉酶和乳酸脱氢酶(LDH)的释放。用AR42J细胞培养基的1 ml上清液刺激大鼠巨噬细胞。最后,检测巨噬细胞的核因子κB激活以及肿瘤坏死因子-α和白细胞介素-1β分泌。

结果

C组胀亡细胞增加而凋亡细胞减少(P < 0.05);D组细胞出现相反变化。淀粉酶和LDH的释放与胀亡的发生直接相关。C组转录因子核因子κB被激活,肿瘤坏死因子-α和白细胞介素-1β的分泌显著高于B组(P < 0.05);在D组,这些作用显著低于B组(P < 0.05)。这种趋势与淀粉酶和LDH产生的变化一致。

结论

胰腺腺泡细胞死亡模式、细胞内容物释放与巨噬细胞炎症反应之间存在密切关系。

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