Emodin ameliorates acute lung injury induced by severe acute pancreatitis through the up‐regulated expressions of AQP1 and AQP5 in lung

Xu, Jianguo; Huang, Bo; Wu, Yu; Tong, Caiyu; Xie, Peng; Fan, Rong; Gao, Zhenming

doi:10.1111/1440-1681.12627

Cited by 33 publications

(29 citation statements)

References 29 publications

(56 reference statements)

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“…Aquaporin-1 (AQP1) is protein that functioned as water transport across cell membranes that mainly expressed in alveolus capillary endothelial cells. A number of studies have shown that AQP1 might play an important role in the pathogenesis of ALI, and the decreased lung AQP1 expression was closely related to the development of ALI, while the upregulated the expression of AQP1 could ameliorate ALI [ 7 , 8 ].…”

Section: Instructionmentioning

confidence: 99%

Long non-coding RNA CASC2 improved acute lung injury by regulating miR-144-3p/AQP1 axis to reduce lung epithelial cell apoptosis

Shi

Gao

et al. 2018

Cell Biosci

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Background and objectiveApoptosis of lung epithelial cell is implicated in the pathogenesis of acute lung injury (ALI). To study the protective effect and mechanism of cancer susceptibility candidate 2 (CASC2) on reducing lung epithelial cell apoptosis after LPS inducing acute lung injury in mice.Methods and resultsThe ALI mice model was performed by intratracheally instilling with lipopolysaccharide (LPS). The CASC2 expression detected by quantitative real-time polymerase chain reaction was significantly decreased in LPS-induced A549 cell and ALI mice model. LPS induced A549 cell apoptosis, while transfection with pcDNA-CASC2 reversed the increased cell apoptosis, suggesting overexpression of CASC2 inhibited LPS-induced A549 cell apoptosis. In addition, we found that miR-144-3p expression were opposite to CASC2, while Aquaporin-1 (AQP1) expression was opposite to miR-144-3p in LPS-induced A549 cell and ALI mice model. The RNA immunoprecipitation and RNA pull-down assay demonstrated that CASC2 could function as a miR-144-3p decoy. The luciferase reporter assay revealed that AQP1 was a target of miR-144-3p in A549 cell. And then, further in vitro studied showed that CASC2 controlled AQP1 expression by regulating miR-144-3p, and LPS induced A549 cell apoptosis by regulating CASC2/miR-144-3p/AQP1 axis. At last, after injection with lentivirus-expressing CASC2 or control lentivirus, the mice were intratracheally instilled with LPS. Comparing to the mice injected with pcDNA, the mice injected with pcDNA-CASC2 had a significantly reduced lung wet–dry weight ratio.ConclusionsLong non-coding RNA CASC2 improved acute lung injury by regulating miR-144-3p/AQP1 axis to reduce lung epithelial cell apoptosis.

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Section: Instructionmentioning

confidence: 99%

Long non-coding RNA CASC2 improved acute lung injury by regulating miR-144-3p/AQP1 axis to reduce lung epithelial cell apoptosis

Shi

Gao

et al. 2018

Cell Biosci

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“…Emodin has a protective effect in pancreatitis-associated secondary organ damage (Wang et al, 2007; Ning et al, 2009; Xia et al, 2010; Xu et al, 2016), which is both a common serious SAP complication and a main cause of death. Pancreatitis-associated lung injury occurs as a consequence of significant pulmonary hyperemia, edema, and inflammatory infiltration in the lung tissues.…”

Section: Pleiotropic Natural Productsmentioning

confidence: 99%

“…Although the strategies in prevention and treatments have been improved, ALI still causes more than 50% of deaths in SAP (Bhatia, 2002). Emodin attenuates pulmonary edema and enhances alveolar epithelial barrier function by up-regulating the expression of claudin-4, claudin-5, occludin, AQP1, and AQP5 in lung tissue samples from rats with SAP-induced ALI (Xia et al, 2010; Xu et al, 2016). Several in vivo investigations have proposed that emodin can prevent the translocation of bacteria and endotoxins and promote the recovery of intestinal barrier function via inhibiting the intestinal mucosa cell apoptosis and up-regulating the serum leptin content (Ning et al, 2009).…”

Section: Pleiotropic Natural Productsmentioning

confidence: 99%

Chinese Herbal Medicines Attenuate Acute Pancreatitis: Pharmacological Activities and Mechanisms

Xiang

Zhang

et al. 2017

Front. Pharmacol.

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Acute pancreatitis (AP) is a commonly occurring gastrointestinal disorder. An increase in the annual incidence of AP has been observed, and it causes acute hospitalization and high mortality. The diagnosis and treatment guidelines for AP recommend conservative medical treatments focused on reducing pancreatic secretion and secondary injury, as a primary therapeutic approach. Unfortunately, the existing treatment options have limited impact on the incidence and severity of AP due to the complex and multifaceted pathological process of this disease. In recent decades, Chinese herbal medicines (CHMs) have been used as efficient therapeutic agents to attenuate AP in Asian countries. Despite early cell culture, animal models, and clinical trials, CHMs are capable of interacting with numerous molecular targets participating in the pathogenesis of AP; however, comprehensive, up-to-date communication in this field is not yet available. This review focuses on the pharmacological activities of CHMs against AP in vitro and in vivo and the underlying mechanisms. A computational prediction of few selected and promising plant-derived molecules (emodin, baicalin, resveratrol, curcumin, ligustrazine, and honokiol) to target numerous proteins or networks involved in AP was initially established based on a network pharmacology simulation. Moreover, we also summarized some potential toxic natural products for pancreas in order to more safe and reasonable medication. These breakthrough findings may have important implications for innovative drug research and the future development of treatments for AP.

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“…Matsuda et al ( 33 ) demonstrated that FK866 protects against ALI in C57BL/6J mice subjected to intestinal ischemia and reperfusion injury. Emodin has previously been reported to be effective in SAP treatment ( 34 ); however, the underlying mechanism remains unclear. The present study indicated that emodin and FK866 significantly ameliorated histopathological alterations induced by SAP-associated ALI in the lung and pancreatic tissues, as determined by HE staining.…”

Section: Discussionmentioning

confidence: 99%

Emodin alleviates severe acute pancreatitis-associated acute lung injury by decreasing pre-B-cell colony-enhancing factor expression and promoting polymorphonuclear neutrophil apoptosis

Cui

Shu

Xu³

et al. 2017

Molecular Medicine Reports

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The present study aimed to evaluate the protective effects of emodin on severe acute pancreatitis (SAP)-associated acute lung injury (ALI), and investigated the possible mechanism involved. SAP was induced in Sprague-Dawley rats by retrograde infusion of 5% sodium taurocholate (1 ml/kg), after which, rats were divided into various groups and were administered emodin, FK866 [a competitive inhibitor of pre-B-cell colony-enhancing factor (PBEF)] or dexamethasone (DEX). DEX was used as a positive control. Subsequently, PBEF expression was detected in polymorphonuclear neutrophils (PMNs) isolated from rat peripheral blood by reverse transcription-quantitative polymerase chain reaction and western blotting. In addition, histological alterations, apoptosis in lung/pancreatic tissues, apoptosis of peripheral blood PMNs and alterations in the expression of apoptosis-associated proteins were examined by hematoxylin and eosin staining, terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling assay, Annexin V/propidium iodide (PI) assay and western blotting, respectively. Serum amylase activity and wet/dry (W/D) weight ratios were also measured. An in vitro study was also conducted, in which PMNs were obtained from normal Sprague-Dawley rats and were incubated with emodin, FK866 or DEX in the presence of lipopolysaccharide (LPS). Apoptosis of PMNs and the expression levels of apoptosis-associated proteins were examined in cultured PMNs in vitro by Annexin V/PI assay and western blotting, respectively. The results demonstrated that emodin, FK866 and DEX significantly downregulated PBEF expression in peripheral blood PMNs. In addition, emodin, FK866 and DEX reduced serum amylase activity, decreased lung and pancreas W/D weight ratios, alleviated lung and pancreatic injuries, and promoted PMN apoptosis by regulating the expression of apoptosis-associated proteins: Fas, Fas ligand, B-cell lymphoma (Bcl)-2-associated X protein, cleaved caspase-3 and Bcl-extra-large. In addition, the in vitro study demonstrated that emodin, FK866 and DEX significantly reversed the LPS-induced decrease of apoptosis in PMNs by regulating the expression of apoptosis-associated proteins. In conclusion, the present study demonstrated that emodin may protect against SAP-associated ALI by decreasing PBEF expression, and promoting PMN apoptosis via the mitochondrial and death receptor apoptotic pathways.

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Emodin ameliorates acute lung injury induced by severe acute pancreatitis through the up‐regulated expressions of AQP1 and AQP5 in lung

Cited by 33 publications

References 29 publications

Long non-coding RNA CASC2 improved acute lung injury by regulating miR-144-3p/AQP1 axis to reduce lung epithelial cell apoptosis

Long non-coding RNA CASC2 improved acute lung injury by regulating miR-144-3p/AQP1 axis to reduce lung epithelial cell apoptosis

Chinese Herbal Medicines Attenuate Acute Pancreatitis: Pharmacological Activities and Mechanisms

Emodin alleviates severe acute pancreatitis-associated acute lung injury by decreasing pre-B-cell colony-enhancing factor expression and promoting polymorphonuclear neutrophil apoptosis

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