Next Article in Journal
Wound-Healing Peptides for Treatment of Chronic Diabetic Foot Ulcers and Other Infected Skin Injuries
Previous Article in Journal
Novel Bioactive Paulomycin Derivatives Produced by Streptomyces albus J1074
Article Menu
Issue 10 (October) cover image

Export Article

Open AccessArticle
Molecules 2017, 22(10), 1754;

Emodin Inhibition of Influenza A Virus Replication and Influenza Viral Pneumonia via the Nrf2, TLR4, p38/JNK and NF-kappaB Pathways

Department of Microbiology and Immunology, Shantou University Medical College, Shantou 515041, China
Department of Veterinary Medicine, University of Maryland, College Park, and Virginia-Maryland Regional College of Veterinary Medicine, College Park, MD 20742, USA
Author to whom correspondence should be addressed.
Received: 18 September 2017 / Revised: 16 October 2017 / Accepted: 16 October 2017 / Published: 18 October 2017
View Full-Text   |   Download PDF [7712 KB, uploaded 18 October 2017]   |  


Lasting activations of toll-like receptors (TLRs), MAPK and NF-κB pathways can support influenza A virus (IAV) infection and promote pneumonia. In this study, we have investigated the effect and mechanism of action of emodin on IAV infection using qRT-PCR, western blotting, ELISA, Nrf2 luciferase reporter, siRNA and plaque inhibition assays. The results showed that emodin could significantly inhibit IAV (ST169, H1N1) replication, reduce IAV-induced expressions of TLR2/3/4/7, MyD88 and TRAF6, decrease IAV-induced phosphorylations of p38/JNK MAPK and nuclear translocation of NF-κB p65. Emodin also activated the Nrf2 pathway, decreased ROS levels, increased GSH levelss and GSH/GSSG ratio, and upregulated the activities of SOD, GR, CAT and GSH-Px after IAV infection. Suppression of Nrf2 via siRNA markedly blocked the inhibitory effects of emodin on IAV-induced activations of TLR4, p38/JNK, and NF-κB pathways and on IAV-induced production of IL-1β, IL-6 and expression of IAV M2 protein. Emodin also dramatically increased the survival rate of mice, reduced lung edema, pulmonary viral titer and inflammatory cytokines, and improved lung histopathological changes. In conclusion, emodin can inhibit IAV replication and influenza viral pneumonia, at least in part, by activating Nrf2 signaling and inhibiting IAV-induced activations of the TLR4, p38/JNK MAPK and NF-κB pathways. View Full-Text
Keywords: influenza A virus; emodin; toll-like receptors (TLRs); MAPK; NF-κB; Nrf2 influenza A virus; emodin; toll-like receptors (TLRs); MAPK; NF-κB; Nrf2

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Supplementary material


Share & Cite This Article

MDPI and ACS Style

Dai, J.-P.; Wang, Q.-W.; Su, Y.; Gu, L.-M.; Zhao, Y.; Chen, X.-X.; Chen, C.; Li, W.-Z.; Wang, G.-F.; Li, K.-S. Emodin Inhibition of Influenza A Virus Replication and Influenza Viral Pneumonia via the Nrf2, TLR4, p38/JNK and NF-kappaB Pathways. Molecules 2017, 22, 1754.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics



[Return to top]
Molecules EISSN 1420-3049 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top