Open Access

Emodin ameliorates acute pancreatitis‑induced lung injury by suppressing NLRP3 inflammasome‑mediated neutrophil recruitment

  • Authors:
    • Nan Jiang
    • Zhaoxia Li
    • Yalan Luo
    • Liu Jiang
    • Guixin Zhang
    • Qi Yang
    • Hailong Chen
  • View Affiliations

  • Published online on: June 9, 2021     https://doi.org/10.3892/etm.2021.10289
  • Article Number: 857
  • Copyright: © Jiang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

Severe acute pancreatitis (SAP) activates the systemic inflammatory response and is potentially lethal. The aim of the present study was to determine the effects of emodin on acute lung injury (ALI) in rats with SAP and investigate the role of the Nod‑like receptor protein 3 (NLRP3) inflammasome and its association with neutrophil recruitment. Sodium taurocholate (5.0%) was used to establish the SAP model. All animals were randomly assigned into four groups: Sham, SAP, emodin and dexamethasone (positive control drug) groups (n=10 mice per group). Histopathology observation of pancreatic and lung tissues was detected by hematoxylin and eosin staining. The levels of serum amylase, IL‑1β and IL‑18 were measured by ELISA. Single‑cell suspensions were obtained from enzymatically digested lung tissues, followed by flow cytometric analysis for apoptosis. In addition, the expression levels of NLRP3 inflammasome‑associated and apoptosis‑associated proteins in lung tissues were measured by western blotting. Moreover, lymphocyte antigen 6 complex locus G6D+ (Ly6G+) cell recruitment was detected using immunohistochemical analysis. The results revealed that emodin markedly improved pancreatic histological injury and decreased the levels of serum amylase, IL‑1β and IL‑18. Pulmonary edema and apoptosis were significantly alleviated by emodin. Additionally, the protein expression levels of intercellular adhesion molecule 1, NLRP3, apoptosis‑associated speck‑like protein containing a CARD and cleaved caspase‑1 were downregulated following emodin treatment. Moreover, emodin inhibited Ly6G+ cell recruitment in lung tissues. The present study demonstrated that emodin may offer protection against ALI induced by SAP via inhibiting and suppressing NLRP3 inflammasome‑mediated neutrophil recruitment and may be a novel therapeutic strategy for the clinical treatment of ALI.
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August-2021
Volume 22 Issue 2

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Jiang N, Li Z, Luo Y, Jiang L, Zhang G, Yang Q and Chen H: Emodin ameliorates acute pancreatitis‑induced lung injury by suppressing NLRP3 inflammasome‑mediated neutrophil recruitment. Exp Ther Med 22: 857, 2021
APA
Jiang, N., Li, Z., Luo, Y., Jiang, L., Zhang, G., Yang, Q., & Chen, H. (2021). Emodin ameliorates acute pancreatitis‑induced lung injury by suppressing NLRP3 inflammasome‑mediated neutrophil recruitment. Experimental and Therapeutic Medicine, 22, 857. https://doi.org/10.3892/etm.2021.10289
MLA
Jiang, N., Li, Z., Luo, Y., Jiang, L., Zhang, G., Yang, Q., Chen, H."Emodin ameliorates acute pancreatitis‑induced lung injury by suppressing NLRP3 inflammasome‑mediated neutrophil recruitment". Experimental and Therapeutic Medicine 22.2 (2021): 857.
Chicago
Jiang, N., Li, Z., Luo, Y., Jiang, L., Zhang, G., Yang, Q., Chen, H."Emodin ameliorates acute pancreatitis‑induced lung injury by suppressing NLRP3 inflammasome‑mediated neutrophil recruitment". Experimental and Therapeutic Medicine 22, no. 2 (2021): 857. https://doi.org/10.3892/etm.2021.10289