Basic Study
Copyright ©The Author(s) 2018. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Jan 7, 2018; 24(1): 35-45
Published online Jan 7, 2018. doi: 10.3748/wjg.v24.i1.35
Emodin and baicalein inhibit sodium taurocholate-induced vacuole formation in pancreatic acinar cells
Jun Li, Rui Zhou, Bei-Bei Bie, Na Huang, Ying Guo, Hai-Yan Chen, Meng-Jiao Shi, Jun Yang, Jian Zhang, Zong-Fang Li
Jun Li, Rui Zhou, Bei-Bei Bie, Na Huang, Ying Guo, Hai-Yan Chen, Meng-Jiao Shi, Jun Yang, Jian Zhang, Zong-Fang Li, National and Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, the Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710004, Shaanxi Province, China
Author contributions: Li J and Zhou R contributed equally to this work; Li J, Zhou R and Li ZF designed the research; Li J and Zhou R performed the research; Bie BB, Huang N, Guo Y, Chen HY and Shi MJ contributed new reagents/analytic tools; Li J, Zhou R, Yang J and Zhang J analyzed the data; Li J, Zhou R, Zhang J and Li ZF wrote the paper.
Supported by the National Natural Science Foundation of China, No. 30901945; Science Research Foundation of Shaanxi Administration of Traditional Chinese Medicine, No. 15-ZY029; and Science Research Foundation of the Second Affiliated Hospital of Xi’an Jiaotong University, No. RC(XM)201602.
Institutional review board statement: This study was approved by the Ethics Committee of the Second Affiliated Hospital of Xi’an Jiaotong University (Xi’an, China).
Institutional animal care and use committee statement: All animal procedures were approved by the Institutional Animal Care and Use Committee of Xi’an Jiaotong University Health Science Center and performed according to the National Guide for the Care and Use of Laboratory Animals.
Conflict-of-interest statement: The authors declare no conflicts of interest.
Data sharing statement: No additional unpublished data are available.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Zong-Fang Li, MD, PhD, National and Local Joint Engineering Research Center of Biodiagnostics and Biotherapy, the Second Affiliated Hospital of Xi’an Jiaotong University, Xi’an 710004, Shaanxi Province, China. lzf2568@xjtu.edu.cn
Telephone: +86-29-87678002 Fax: +86-29-87678634
Received: August 31, 2017
Peer-review started: September 3, 2017
First decision: September 27, 2017
Revised: November 23, 2017
Accepted: November 27, 2017
Article in press: November 27, 2017
Published online: January 7, 2018
Processing time: 128 Days and 19.7 Hours
Abstract
AIM

To investigate the effects of combined use of emodin and baicalein (CEB) at the cellular and organism levels in severe acute pancreatitis (SAP) and explore the underlying mechanism.

METHODS

SAP was induced by retrograde infusion of 5% sodium taurocholate into the pancreatic duct in 48 male SD rats. Pancreatic histopathology score, serum amylase activity, and levels of tumour necrosis factor alpha (TNF-α), interleukin 6 (IL-6), and IL-10 were determined to assess the effects of CEB at 12 h after the surgery. The rat pancreatic acinar cells were isolated from healthy male SD rats using collagenase. The cell viability, cell ultrastructure, intracellular free Ca2+ concentration, and inositol (1,4,5)-trisphosphate receptor (IP3R) expression were investigated to assess the mechanism of CEB.

RESULTS

Pancreatic histopathology score (2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05) and serum amylase activity (2866.2 ± 617.7 vs 5241.3 ± 1410.0, P < 0.05) were significantly decreased in the CEB (three doses) treatment group compared with the SAP group (2.07 ± 1.20 vs 6.84 ± 1.13, P < 0.05). CEB dose-dependently reduced the levels of the pro-inflammatory cytokines IL-6 (466.82 ± 48.55 vs 603.50 ± 75.53, P < 0.05) and TNF-α (108.04 ± 16.10 vs 215.56 ± 74.67, P < 0.05) and increased the level of the anti-inflammatory cytokine IL-10 (200.96 ± 50.76 vs 54.18 ± 6.07, P < 0.05) compared with those in the SAP group. CEB increased cell viability, inhibited cytosolic Ca2+ concentration, and significantly ameliorated intracellular vacuoles and IP3 mRNA expression compared with those in the SAP group (P < 0.05). There was a trend towards decreased IP3R protein in the CEB treatment group; however, it did not reach statistical significance (P > 0.05).

CONCLUSION

These results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that CEB is a suitable approach for SAP treatment.

Keywords: Inositol (1,4,5)-trisphosphate receptor; Severe acute pancreatitis; Calcium overload; Emodin; Baicalein; Pancreatic acinar cell

Core tip: Combined use of emodin and baicalein (CEB) was found to act on key aspects of severe acute pancreatitis (SAP) pathogenesis; it regulated inflammatory factors and inhibited calcium overload, which underlie this synergy. These results at the cellular and organism levels reflect a preliminary mechanism of CEB in SAP and indicate that the development of CEB is promising for the treatment of patients with SAP.