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越婢汤对急性肺肾损伤重症急性胰腺炎大鼠水代谢的影响。

Effects of Yue-Bi-Tang on water metabolism in severe acute pancreatitis rats with acute lung-kidney injury.

机构信息

Department of Integrative Medicine, West China Hospital, Sichuan University, Chengdu 610041, Sichuan Province, China.

Department of Traditional Chinese Medicine, Xiang'an Hospital of Xiamen University, Xiamen 361101, Fujian Province, China.

出版信息

World J Gastroenterol. 2020 Nov 21;26(43):6810-6821. doi: 10.3748/wjg.v26.i43.6810.

DOI:10.3748/wjg.v26.i43.6810
PMID:33268963
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7684462/
Abstract

BACKGROUND

The complications acute lung injury and acute kidney injury caused by severe inflammation are the main reasons of high mortality of severe acute pancreatitis (SAP). These two complications can both lead to water metabolism and acid-base balance disorders, which could act as additional critical factors affecting the disease trend. Aquaporins (AQPs), which can regulate the transmembrane water transport, have been proved to participate in the pathophysiological process of SAP and the associated complications, such as acute lung injury and acute kidney injury. Thus, exploring herbs that can effectively regulate the expression of AQP in SAP could benefit the prognosis of this disease.

AIM

To determine whether Yue-Bi-Tang (YBT) can regulate the water metabolism in rats with severe acute pancreatitis regulating the expression of aquaporins.

METHODS

Sprague-Dawley rats were randomly divided into three groups, sham operation group (SOG), model group (MG), and treatment group (TG). SAP was induced with 3.5% sodium taurocholate in the MG and TG. Rats in the TG were administered with YBT while SOG and MG rats were given the same volume of saline. Blood and tissue samples were harvested to detect serum inflammatory cytokines, histopathological changes, malondialdehyde and superoxide dismutase in the lung, and protein and mRNA expression of kidney injury molecule-1, α-smooth muscle actin, and vimentin in the kidney, and AQP1 and 4 in the lung, pancreas, and kidney.

RESULTS

The serum interleukin-10, tumor necrosis factor α, and creatinine levels were higher in the MG than in the SOG. Tumor necrosis factor α level in the TG was lower than that in the MG. Malondialdehyde level in lung tissues was higher than in the SOG. The pathological scores and edema scores of the pancreas, lung, and kidney tissues in the MG were all higher than those in the SOG and TG. The protein expression of AQP4 in lung tissues and AQP1 in kidney tissues in the MG were higher than those in the SOG and TG. The expression of vimentin was significantly higher in the MG than in the SOG. The expression of mRNA in the lung and kidney, and mRNA in the kidney was up-regulated in the MG compared to the SOG.

CONCLUSION

YBT might regulate water metabolism to reduce lung and kidney edema of SAP rats decreasing AQP expression, and alleviate the tissue inflammatory injury.

摘要

背景

严重炎症引起的急性肺损伤和急性肾损伤是重症急性胰腺炎(SAP)高死亡率的主要原因。这两种并发症均可导致水代谢和酸碱平衡紊乱,成为影响疾病趋势的附加关键因素。水通道蛋白(AQP)可调节跨膜水转运,已被证明参与 SAP 及相关并发症(如急性肺损伤和急性肾损伤)的病理生理过程。因此,探索能有效调节 SAP 中 AQP 表达的草药可能有利于改善该病的预后。

目的

确定越婢汤(YBT)是否能通过调节水通道蛋白的表达来调节重症急性胰腺炎大鼠的水代谢。

方法

SD 大鼠随机分为三组:假手术组(SOG)、模型组(MG)和治疗组(TG)。MG 和 TG 大鼠采用 3.5%牛磺胆酸钠诱导 SAP,TG 大鼠给予 YBT,SOG 和 MG 大鼠给予等体积生理盐水。采集血样和组织样本,检测血清炎症细胞因子、肺组织病理变化、丙二醛和超氧化物歧化酶,检测肾组织中肾损伤分子-1、α-平滑肌肌动蛋白和波形蛋白的蛋白和 mRNA 表达,以及肺、胰腺和肾脏中 AQP1 和 AQP4 的表达。

结果

MG 组血清白细胞介素-10、肿瘤坏死因子-α和肌酐水平高于 SOG 组,TG 组肿瘤坏死因子-α水平低于 MG 组。肺组织丙二醛水平高于 SOG 组。MG 组胰腺、肺和肾脏组织的病理评分和水肿评分均高于 SOG 和 TG 组。MG 组肺组织 AQP4 蛋白表达和肾组织 AQP1 蛋白表达均高于 SOG 和 TG 组,MG 组 vimentin 表达明显高于 SOG 组。MG 组肺和肾组织 mRNA 表达及肾组织 mRNA 表达均高于 SOG 组。

结论

YBT 可能通过调节水代谢来减轻 SAP 大鼠的肺和肾水肿,降低 AQP 表达,减轻组织炎症损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/bfdcc21b87e2/WJG-26-6810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/a993f1784dc9/WJG-26-6810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/13790add7f78/WJG-26-6810-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/42db83036814/WJG-26-6810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/bfdcc21b87e2/WJG-26-6810-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/a993f1784dc9/WJG-26-6810-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/13790add7f78/WJG-26-6810-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/42db83036814/WJG-26-6810-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/53d3/7684462/bfdcc21b87e2/WJG-26-6810-g004.jpg

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