CORRECTION article

Front. Pharmacol., 05 May 2020

Sec. Gastrointestinal and Hepatic Pharmacology

Volume 11 - 2020 | https://doi.org/10.3389/fphar.2020.00569

Corrigendum: TSG-6 Inhibits Oxidative Stress and Induces M2 Polarization of Hepatic Macrophages in Mice With Alcoholic Hepatitis via Suppression of STAT3 Activation

  • YW

    Yue-Meng Wan 1,2

  • HW

    Hua-Mei Wu 1

  • YL

    Yu-Hua Li 1

  • ZX

    Zhi-Yuan Xu 1

  • JY

    Jin-Hui Yang 1

  • CL

    Chang Liu 2

  • YH

    Yue-Feng He 2

  • MW

    Men-Jie Wang 2

  • XW

    Xi-Nan Wu 2*

  • YZ

    Yuan Zhang 3

  • 1. Gastroenterology Department, The 2nd Affiliated Hospital of Kunming Medical University, Kunming, China

  • 2. Department of Occupational, Labor and Environmental Health, Public Health Institute of Kunming Medical University, Kunming, China

  • 3. The Biomedical Engineering Research Center, Kunming Medical University, Kunming, China

In the original article, there was a mistake in Figure 2 as published. Two microphotos (A, C) were mistakenly inserted. The corrected Figure 2 appears below.

Figure 2

In addition, there were two errors in the Abstract. In the second sentence, the word “effective” was used. The correct word is “effects.” In the tenth sentence, the word "were" was used. The correct word was "was." Corrections have been made to the Abstract:

“Tumor necrosis factor (TNF)-α-stimulated protein 6 (TSG-6) is a secreted protein with diverse tissue protective and anti-inflammatory properties. We aimed to investigate its effects in treating mice with alcoholic hepatitis (AH) and the associated mechanisms. AH was induced in 8–10 week female C57BL/6N mice by chronic-binge ethanol feeding for 10 days. Intraperitoneal (i.p.) injection of recombinant mouse TSG-6 or saline were performed in mice on day 10. Blood samples and hepatic tissues were collected on day 11. Biochemistry, liver histology, flow cytometry, and cytokine measurements were conducted. Compared to the normal control mice, the AH mice had significantly increased liver/body weight ratio, serum alanine aminotransferase (ALT) and aspartate aminotransferases (AST), hepatic total cholesterol (TC), triglyceride (TG), malondialdehyde (MDA), hepatic macrophage infiltration, serum and hepatic interleukin (IL)-6, and tumor necrosis factor (TNF)-α, which were markedly reduced by i.p. injection of rmTSG-6. Compared to the normal control mice, the hepatic glutathione (GSH), accumulation of M2 macrophages, serum, and hepatic IL-10 and TSG-6 were prominently reduced in the AH mice, which were significantly enhanced after i.p. injection of rmTSG-6. Compared to the normal control mice, hepatic activation of signal transducer and activator of transcription 3 (STAT3) as significantly induced, which was markedly suppressed by rmTSG-6 treatment. TSG-6 was effective for the treatment of AH mice, which might be associated with its ability in inhibiting hepatic oxidative stress and inducing hepatic M2 macrophages polarization via suppressing STAT3 activation.”

The authors apologize for these errors and state that they do not change the scientific conclusions of the article in any way. The original article has been updated.

Summary

Keywords

TSG-6, alcoholic hepatitis, oxidative stress, macrophage polarization, STAT3 activation

Citation

Wan Y-M, Wu H-M, Li Y-H, Xu Z-Y, Yang J-H, Liu C, He Y-F, Wang M-J, Wu X-N and Zhang Y (2020) Corrigendum: TSG-6 Inhibits Oxidative Stress and Induces M2 Polarization of Hepatic Macrophages in Mice With Alcoholic Hepatitis via Suppression of STAT3 Activation. Front. Pharmacol. 11:569. doi: 10.3389/fphar.2020.00569

Received

02 March 2020

Accepted

15 April 2020

Published

05 May 2020

Volume

11 - 2020

Edited and reviewed by

Raffaele Capasso, University of Naples Federico II, Italy

Updates

Copyright

*Correspondence: Xi-Nan Wu,

This article was submitted to Gastrointestinal and Hepatic Pharmacology, a section of the journal Frontiers in Pharmacology

Disclaimer

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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