Department of General Surgery, Renmin Hospital of Wuhan University, 238 Jiefang Road, Wuhan, 430060, Hubei Province, China.
Inflammation. 2012 Feb;35(1):11-22. doi: 10.1007/s10753-010-9284-2.
We hypothesize that adrenal insufficiency in acute necrotizing pancreatitis (ANP) is attributable to hemorrhagic inflammation, necrosis, and apoptosis of the adrenal cortex. Arguments to support this view are presented in the study that investigated morphological and functional changes of adrenal and the distinct roles of inflammatory mediator secretory phospholipase A(2) (sPLA(2)) and apoptosis-related genes Bax and Bcl-2 played in acute adrenal injury in ANP. After ANP model was induced, pancreatic histology, serum amylase, sPLA(2), and corticosterone were analyzed. The adrenal morphology, apoptotic cells by TUNEL assay, and ultrastructures were observed. sPLA(2)-IIA and Bcl-2 and Bax expressions were detected by immunohistochemistry. Histopathologic grading of adrenal was higher in ANP group than in controls. Serum corticosterone was stimulated to maximal level at 3 h, then dropped to the bottom at 24 h (P<0.05). Apoptotic index, sPLA2-IIA, and Bax expression were increased steeply after pancreatitis, and the Bax/Bcl-2 ratio was elevated gradually (P<0.05). Sustained decrease in serum corticosterone level following adrenal injury during ANP appears to be, in part, due to the crucial roles of inflammation and apoptosis in adrenal cortex. These findings could suggest that sPLA2, Bax, and Bcl-2 may be involved in the course of adrenal injury after ANP.
我们假设急性坏死性胰腺炎（ANP）中的肾上腺功能不全归因于肾上腺皮质的出血性炎症、坏死和细胞凋亡。本研究通过研究 ANP 中肾上腺的形态和功能变化以及炎症介质分泌型磷脂酶 A2（sPLA2）和凋亡相关基因 Bax 和 Bcl-2 的不同作用，为这一观点提供了依据。在诱导 ANP 模型后，分析了胰腺组织学、血清淀粉酶、sPLA2 和皮质酮。观察了肾上腺形态、TUNEL 检测的凋亡细胞和超微结构。通过免疫组织化学检测 sPLA2-IIA、Bcl-2 和 Bax 的表达。与对照组相比，ANP 组的肾上腺组织病理学分级更高。血清皮质酮在 3 小时达到最大值，然后在 24 小时降至最低（P<0.05）。在胰腺炎后，凋亡指数、sPLA2-IIA 和 Bax 表达急剧增加，Bax/Bcl-2 比值逐渐升高（P<0.05）。在 ANP 期间，肾上腺损伤后血清皮质酮水平持续下降，部分原因可能是炎症和凋亡在肾上腺皮质中起关键作用。这些发现表明 sPLA2、Bax 和 Bcl-2 可能参与了 ANP 后肾上腺损伤的过程。
