Emodin, a Naturally Occurring Anthraquinone, Ameliorates Experimental Autoimmune Myocarditis in Rats

Song, Zhanchun; Wang, Zhansheng; Bai, Jinghui; Zhao, Li; Hu, Jinglu

doi:10.1620/tjem.228.83

Cited by 6 publications

(11 citation statements)

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“…Emodin is a natural product and is mostly found in roots and barks of many plants, molds, and lichens. 15) Several studies have reported that emodin can ameliorate myocarditis. 15,16,21) In this study, we aimed to investigate the regulatory mechanism of emodin on LPS-induced inflammatory injury in cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

“…15) Several studies have reported that emodin can ameliorate myocarditis. 15,16,21) In this study, we aimed to investigate the regulatory mechanism of emodin on LPS-induced inflammatory injury in cardiomyocytes. We found that LPS reduced H9c2 cells viability and down-regulated the expression of CyclinD1.…”

Section: Discussionmentioning

confidence: 99%

“…The chemical structure of emodin is shown in Figure 1A. Various concentrations (1,5,10,15, and 20 μM) of emodin were used to treat H9c2 cells, and the cytotoxicity of emodin was evaluated by testing cell viability. CCK-8 results ( Figure 1B) suggested that cell viability was unaffected by 0, 1, 5, 10, and 15 μM of emodin, as compared with the control group (P > 0.05).…”

Section: High Concentration Of Emodin Decreased H9c2 Cells Viabilitymentioning

confidence: 99%

“…12) Besides, emodin has been recognized as an antiinflammatory, anti-fibrosis, and anti-atherosclerosis agent. [13][14][15] Further, Chen, et al reported that emodin attenuated tumor necrosis factor-alpha (TNF-α)-induced apoptosis and autophagy in mice C2C12 cells. 16) The research of Jiang et al displayed that emodin downregulated the expression of interleukin-17 (IL-17) and exerted myocardioprotective effects on the mice with viral myocarditis.…”

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confidence: 99%

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Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells

Yang¹,

Jiang²,

Zhuge³

2019

Int. Heart J.

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Emodin is a natural product extracted from Rheum palmatum. There are few recent studies on emodin in the treatment of myocarditis. This study aimed to investigate the effect of emodin on lipopolysaccharide (LPS)induced inflammatory injury in cardiomyocytes. H9c2 cells were treated with 10 μM of LPS and different concentrations (0, 1, 5, 10, 15, and 20 μM) of emodin. The expression of miR-223 was changed by transient transfection. Thereafter, cell viability, apoptosis, the expression of CyclinD1 and Jnk-associated proteins, and the release of pro-inflammatory factors were assessed by cell Counting Kit-8, flow cytometry analysis, quantitative real-time polymerase chain reaction Western blot, and enzyme-linked immunosorbent assay respectively. The results showed that 20 μM of emodin significantly decreased H9c2 cells viability. LPS significantly damaged H9c2 cells, as cell viability was reduced, CyclinD1 was down-regulated, apoptosis was induced, the release of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-alpha were increased, and the phosphorylation of Jnk and c-Jun were promoted. Emodin protected H9c2 cells against LPS-induced inflammatory injury. miR-223 expression was significantly up-regulated by LPS exposure, while emodin lessened this up-regulation. LPS-injured H9c2 cells were attenuated by the overexpression of miR-223; emodin has protective actions on LPS-injured H9c2 cells and targets. Besides, SP600125 (an inhibitor of Jnk) eliminated miR-223-modulated inflammatory injury in H9c2 cells. These data demonstrated that emodin could attenuate LPS-induced inflammatory injury and deactivate Jnk signaling pathway through down-regulation of miR-223. (Int Heart J 2019; 60: 436-443)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: High Concentration Of Emodin Decreased H9c2 Cells Viabilitymentioning

confidence: 99%

mentioning

confidence: 99%

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Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells

Yang¹,

Jiang²,

Zhuge³

2019

Int. Heart J.

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“…Emodin is an important component of traditional Chinese herbs and has well-documented anti-inflammatory effect (Song et al, 2012). It has been shown to possess several biological activities like immuneosuppressive (Zhao et al, 2012) and as a useful chemotherapeutic agent against hepatocellular carcinoma (Jeon et al, 2012).…”

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confidence: 99%

Protective Efficacy of Emodin against γ-Rays Induced Acute Hepatorenal Injury in Rats

2012

Egypt. J. Rad.Sci.

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MODIN(C 16 H 12 O 5), an active principle extracted from Rheum palmatum. Its protective effect was evaluated against γ-rays-induced biochemical alterations in rats. The purpose of recent study is to demonstrate protective efficacy of emodin against γ-rays induced acute hepatorenal injury in rats. γ-irradiation (6 Gy) caused significant elevation in the release of serum alanine and aspartate transaminases, (ALT & AST), alkaline phosphatase (SALP), lactate dehydrogenase (LDH), bilirubin (Br) and glucose (Gu) with concomitant decrease in haemoglobin (Hb) after 24 h of its exposure. Toxicant exposure intensified the lipid peroxidation (LPO, measured as MDA units), total cholesterol (TC) and activity of acid phosphatase (TAC) and altered glutathione status (GSH), activities of adenosine triphosphatase (ATP), alkaline phosphatase (TALP), glutamate dehydrogenase (GDH) as well as major cellular constituents; total proteins (TP) and glycogen (Gn) in liver and kidney, compared to control measures. Emodin, oral treatment, significantly lessened the toxicity by protecting γ-rays-induced alterations in various blood and tissue biochemical variables, compared to irradiated groups. Thus, the study concluded that emodin at a dose of 40 mg/ kg body wt possesses optimum hepatorenal protective ability in γ-irradiated toxicant rats.

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Emodin alleviates LPS‐induced myocardial injury through inhibition of NLRP3 inflammasome activation

Dai

Chen

et al. 2021

Phytotherapy Research

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Myocardial injury and cardiovascular dysfunction are serious consequences of sepsis and contribute to high mortality. Currently, the pathogenesis of myocardial injury in sepsis is still unclear, and therapeutic approaches are limited. In this study, we investigated the protective effect of emodin on septic myocardial injury and the underlying mechanism. Lipopolysaccharide (LPS)‐induced C57BL/6 mice and cardiomyocytes were used as models of sepsis in vivo and in vitro, respectively. The results showed that emodin alleviated cardiac dysfunction, myocardial injury and improved survival rate in LPS‐induced septic mice. Emodin attenuated the levels of inflammatory cytokines and cardiac inflammation induced by LPS. Emodin reduced NOD‐like receptor protein 3 (NLRP3) and Gasdermin D (GSDMD) expression in the heart tissue of LPS‐induced septic mice. In vitro, emodin alleviated LPS‐induced cell injury and inflammation in cardiomyocytes by inhibiting NLRP3 inflammasome activation. In addition, an NLRP3 inhibitor was used to further confirm the function of the NLRP3 inflammasome in LPS‐induced myocardial injury. Taken together, our findings suggest that emodin improves LPS‐induced myocardial injury and cardiac dysfunction by alleviating the inflammatory response and cardiomyocyte pyroptosis by inhibiting NLRP3 inflammasome activation, which provides a feasible strategy for preventing and treating myocardial injury in sepsis.

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Emodin, a Naturally Occurring Anthraquinone, Ameliorates Experimental Autoimmune Myocarditis in Rats

Abstract: In the version of this article published in the July issue, 2012, the lettering of 'β-action' is a misprint for 'GAPDH' in panel A of Figure 2 (pages 228).

Cited by 6 publications

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Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells

Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells

Protective Efficacy of Emodin against γ-Rays Induced Acute Hepatorenal Injury in Rats

Emodin alleviates LPS‐induced myocardial injury through inhibition of NLRP3 inflammasome activation

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