Emodin and Its Role in Chronic Diseases

Monisha, B. Anu; Kumar, Niraj; Tiku, Ashu Bhan

doi:10.1007/978-3-319-41334-1_3

Cited by 61 publications

(40 citation statements)

References 151 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…21 Emodin has anti-inflammatory and antibacterial, antioxidant and antiviral efficacys. 22 A research displayed that emodin restrained airway inflammatory damage in mouse. 23 Other research proposed that emodin could reduce the inflammatory response caused by influenza A virus by restraining the levels of inflammatory factors.…”

Section: Discussionmentioning

confidence: 99%

Retracted: Emodin relieved lipopolysaccharide‐evoked inflammatory damage in WI‐38 cells by up‐regulating taurine up‐regulated gene 1

et al. 2020

View full text Add to dashboard Cite

Background: Neonatal pneumonia (NP) has a high fatality rate in neonatal illness. This research investigated the functions of emodin on lipopolysaccharide (LPS)-evoked inflammatory injury in WI-38 cells. Methods: Cell counting kit-8 (CCK-8) assay and flow cytometry were utilized for examining the impacts of LPS and emodin on viability and apoptosis, respectively. Taurine up-regulated gene 1 (TUG1) level was altered through cell transfection and investigated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Moreover, RT-qPCR, western blot and enzyme-linked immunosorbent assay (ELISA) were utilized for investigating expressions of monocyte chemoattractant protein-1 (MCP-1) and interleukin (IL)-6. Western blot was carried out for investigating the levels of Bcl-2, Bax, pro-Caspase-3, cleaved-Caspase-3 and NF-κB and p38MAPK pathway-related proteins. Results: LPS treatment restrained cell viability, enhanced apoptosis, and expressions of inflammation-related IL-6 and MCP-1. Emodin alleviated LPSevoked inflammatory injury and restrained the NF-κB and p38MAPK pathways. Furthermore, emodin positively regulated TUG1 expression and TUG1 silencing could reverse the efficacy of emodin on IL-6 and MCP-1 expressions. Finally, TUG1 regulates the expression of inflammatory factors through NF-κB and p38MAPK pathways. Conclusion: Emodin alleviated LPS-evoked inflammatory injury by raising TUG1 expression via NF-κB and p38MAPK pathways in WI-38 cells. K E Y W O R D S emodin, inflammatory damage, NF-κB and p38MAPK pathways, neonatal pneumonia, TUG1 1 | INTRODUCTION Neonatal pneumonia (NP) is the most familiar respiratory diseases in the neonatal stage. Most NP is caused by lung infections which are caused by inhalation of

show abstract

Section: Discussionmentioning

confidence: 99%

Retracted: Emodin relieved lipopolysaccharide‐evoked inflammatory damage in WI‐38 cells by up‐regulating taurine up‐regulated gene 1

et al. 2020

View full text Add to dashboard Cite

show abstract

“…The anti-cancer effect of emodin has been reported in several types of cancer; however, the development of novel therapeutic strategies for cancer treatment is required [ 27 ]. In particular, various reports have shown that emodin decreases HCC growth through the suppression of oncogenic growth signaling, such as the MAPK, PI3K-AKT, and STAT3 pathways, in both in vitro and in vivo models [ 9 , 28 , 29 ].…”

Section: Discussionmentioning

confidence: 99%

Emodin Sensitizes Hepatocellular Carcinoma Cells to the Anti-Cancer Effect of Sorafenib through Suppression of Cholesterol Metabolism

Kim

Lee

et al. 2018

IJMS

View full text Add to dashboard Cite

Reduced therapeutic efficacy of sorafenib, a first-generation multikinase inhibitor, is often observed during the treatment of advanced hepatocellular carcinoma (HCC). Emodin is an active component of Chinese herbs, and is effective against leukemia, lung cancer, colon cancer, pancreatic cancer, and HCC; however, the sensitizing effect of emodin on sorafenib-based HCC therapy has not been evaluated. Here, we demonstrate that emodin significantly improved the anti-cancer effect of sorafenib in HCC cells, such as HepG2, Hep3B, Huh7, SK-HEP-1, and PLC/PRF5. Mechanistically, emodin inhibits sterol regulatory element-binding protein-2 (SREBP-2) transcriptional activity, which suppresses cholesterol biosynthesis and oncogenic protein kinase B (AKT) signaling. Additionally, attenuated cholesterol synthesis and oncogenic AKT signaling inactivated signal transducer and activator of transcription 3 (STAT3), an oncogenic transcription factor. Furthermore, emodin synergistically increased cell cycle arrest in the G1 phase and apoptotic cells in the presence of sorafenib. Animal models xenografted with HepG2 or SK-HEP-1 cells also showed that the combination of emodin and sorafenib was sufficient to inhibit tumor growth. Overall, these results suggested that the combination of emodin and sorafenib may offer a potential therapy for patients with advanced HCC.

show abstract

“…105 For example, apigenin from Epimedium koreanum Nakai, emodin from Rheum palmatum L, quercetin from Hypericun ascyron L and curcumin from Curcuma louga L are all reported to modulate various chronic diseases within safe dose range. [106][107][108][109] Here in this article, we systematically review the existing literature concerning coptisine's diverse beneficial properties, and this continues to support the recommendation that coptisine can be applied to the treatment for cancer, inflammation, CVDs and metabolic disorders.…”

Section: Future Pros Pec Tsmentioning

confidence: 98%

Coptisine fromCoptis chinensisexerts diverse beneficial properties: A concise review

Luo

Deng

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

Coptisine is a natural small‐molecular compound extracted from Coptis chinensis (CC) with a history of using for thousands of years. This work aimed at summarizing coptisine's activity and providing advice for its clinical use. We analysed the online papers in the database of SciFinder, Web of Science, PubMed, Google scholar and CNKI by setting keywords as ‘coptisine’ in combination of ‘each pivotal pathway target’. Based on the existing literatures, we find (a) coptisine exerted potential to be an anti‐cancer, anti‐inflammatory, CAD ameliorating or anti‐bacterial drug through regulating the signalling transduction of pathways such as NF‐κB, MAPK, PI3K/Akt, NLRP3 inflammasome, RANKL/RANK and Beclin 1/Sirt1. However, we also (b) observe that the plasma concentration of coptisine demonstrates obvious non‐liner relationship with dosage, and even the highest dosage used in animal study actually cannot reach the minimum concentration level used in cell experiments owing to the poor absorption and low availability of coptisine. We conclude (a) further investigations can focus on coptisine's effect on caspase‐1‐involved inflammasome assembling and pyroptosis activation, as well as autophagy. (b) Under circumstance of promoting coptisine availability by pursuing nano‐ or microrods strategies or applying salt‐forming process to coptisine, can it be introduced to clinical trial.

show abstract

Emodin and Its Role in Chronic Diseases

Cited by 61 publications

References 151 publications

Retracted: Emodin relieved lipopolysaccharide‐evoked inflammatory damage in WI‐38 cells by up‐regulating taurine up‐regulated gene 1

Retracted: Emodin relieved lipopolysaccharide‐evoked inflammatory damage in WI‐38 cells by up‐regulating taurine up‐regulated gene 1

Emodin Sensitizes Hepatocellular Carcinoma Cells to the Anti-Cancer Effect of Sorafenib through Suppression of Cholesterol Metabolism

Coptisine fromCoptis chinensisexerts diverse beneficial properties: A concise review

Contact Info

Product

Resources

About