Emodin alleviates bleomycin-induced pulmonary fibrosis in rats

Guan, Ruijuan; Zhao, Xiaomei; Wang, Xia; Song, Nana; Guo, Yuhong; Yan, Xianxia; Jiang, Liping; Cheng, Wenjing; Shen, Lin‐Lin

doi:10.1016/j.toxlet.2016.10.004

Cited by 41 publications

(27 citation statements)

References 41 publications

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“…Emodin has been reported to exert anti-inflammatory, antitumor, antiviral and immunomodulatory effects ( 27 ). Previous studies have reported that emodin additionally exhibits an antifibrotic effect in a rat lung fibrosis model, in addition to in heart tissue and other organs ( 28 – 30 ). It has been reported that emodin has a protective effect in liver fibrosis ( 20 ).…”

Section: Discussionmentioning

confidence: 97%

Emodin alleviates CCl4‑induced liver fibrosis by suppressing epithelial‑mesenchymal transition and transforming growth factor‑β1 in rats

et al. 2018

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Liver fibrosis is a chronic disease that exhibits a complicated pathophysiology. It is characterized by the deposition of the extracellular matrix. Emodin, an active constituent isolated from rhubarb, has antibacterial, immunosuppressive and anti-inflammatory effects. In the present study, the mechanism through which emodin alleviates liver fibrosis in rats was investigated. A rat model of liver fibrosis was generated by administering CCl4 via subcutaneous injection twice a week for 12 weeks. Emodin or sodium carboxymethylcellulose (CMC), as the vehicle, were intragastrically administered daily. After 12 weeks, the liver function index was examined by blood analysis, histopathological scores of fibrosis was determined by hematoxylin and eosin staining and level of collagen deposition was examined by Masson staining. In addition, protein and RNA samples were collected for further analysis. The results of the present study revealed that emodin significantly reduced the liver function index and level of collagen deposition in a dose-dependent manner. Furthermore, emodin reduced the expression of transforming growth factor-β1 (TGF-β1) and the phosphorylation levels of mothers against decapentaplegic homolog 2/3, and inhibited the CCl4-induced downregulation of E-cadherin and upregulation of the mesenchymal markers, fibronectin and vimentin. The expression levels of TGF-β1, Snail family transcriptional repressor (Snail) 2, Snail, twist-related protein 1 and zinc finger E-box-binding homeobox (ZEB)1 and 2 mRNA were significantly decreased in emodin-treated groups compared with the untreated control. Collectively, the results of the present study suggested that emodin may exert antifibrotic effects via the suppression of TGF-β1 signaling and epithelial-mesenchymal transition.

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Section: Discussionmentioning

confidence: 97%

Emodin alleviates CCl4‑induced liver fibrosis by suppressing epithelial‑mesenchymal transition and transforming growth factor‑β1 in rats

et al. 2018

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“…In the preliminary test, twenty mice were used to determine the 50% mouse lethal dose (MLD 50 ) by the method of Reed and Muench and the test doses of emodin, which we had also referred to the previous reports [ 40 , 50 , 51 ]. During experiment, 80 mice were randomly divided into 5 groups using the random number table and anesthetized by intraperitoneal injection of ketamine (100 mg/kg).…”

Section: Methodsmentioning

confidence: 99%

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

Dai

Wang

et al. 2017

Molecules

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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.

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“…A recent study has shown that emodin alleviates pulmonary fibrosis by increasing the expression of Smad7 and thereby silencing the TGF-β/Smad pathway [ 61 ]. Guan et al found that emodin could inhibit the activation of myofibroblasts by downregulating the phosphorylation of signal transduction and transcriptional activator-3 (STAT3) and further decrease the synthesis of collagen by reducing the expression of heat shock protein-47 (HSP-47) [ 5 , 62 ]. Similarly, emodin also alleviates renal fibrosis by inhibiting the expression of connective tissue growth factor (CTGF) and platelet-derived growth factor (PDGF) and the deposition of Col I and Col III [ 63 ].…”

Section: Pharmacologymentioning

confidence: 99%

What we already know about rhubarb: a comprehensive review

et al. 2020

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Rhubarb (also named Rhei or Dahuang), one of the most ancient and important herbs in traditional Chinese medicine (TCM), belongs to the Rheum L. genus from the Polygonaceae family, and its application can be traced back to 270 BC in "Shen Nong Ben Cao Jing". Rhubarb has long been used as an antibacterial, anti-inflammatory, anti-fibrotic and anticancer medicine in China. However, for a variety of reasons, such as origin, variety and processing methods, there are differences in the effective components of rhubarb, which eventually lead to decreased quality and poor efficacy. Additionally, although some papers have reviewed the relationship between the active ingredients of rhubarb and pharmacologic actions, most studies have concentrated on one or several aspects, although there has been great progress in rhubarb research in recent years. Therefore, this review aims to summarize recent studies on the geographic distribution, taxonomic identification, pharmacology, clinical applications and safety issues related to rhubarb and provide insights into the further development and application of rhubarb in the future.

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Emodin alleviates bleomycin-induced pulmonary fibrosis in rats

Cited by 41 publications

References 41 publications

Emodin alleviates CCl4‑induced liver fibrosis by suppressing epithelial‑mesenchymal transition and transforming growth factor‑β1 in rats

Emodin alleviates CCl4‑induced liver fibrosis by suppressing epithelial‑mesenchymal transition and transforming growth factor‑β1 in rats

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

What we already know about rhubarb: a comprehensive review

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