Emodin suppresses LPS-induced inflammation in RAW264.7 cells through a PPARγ-dependent pathway

Zhu, Tao; Zhang, Wei; Feng, She-Jun; Yu, Hui

doi:10.1016/j.intimp.2016.02.014

Cited by 106 publications

(68 citation statements)

References 32 publications

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“…Inflammatory response is a kind of self-protection and defence mechanism in the face of stimulation. But uncontrolled inflammation can cause tissue damage and even injuries [27]. Our study established an in vitro cell model of pressure ulcers by using LPS to stimulate HaCaT cells.…”

Section: Discussionmentioning

confidence: 99%

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Song

Cui

Zhao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background/aim: Pressure ulcers are a disastrous health issue in which inflammation is involved. Emodin possesses biological properties in inflammation. Our study investigated functions of emodin in lipopolysaccharide (LPS)-treated HaCaT cells. Methods: LPS was used to induce cell inflammation. MTT and flow cytometry were applied for cell viability and apoptosis assays, respectively. Moreover, apoptotic proteins were detected by western blot. Similarly, inflammatory factors and signalling related proteins were also determined by western blot. Results: Emodin increased cell viability and diminished apoptosis in LPS-treated HaCaT cells. Moreover, cleaved-PARP, cleaved-caspase-3 and cleaved-caspase-9 were all downregulated by emodin. Furthermore, inflammatory factors IL-1b, IL-6, Cox-2 and iNOS were inhibited by emodin in LPS-treated cells. In addition, emodin decreased phosphorylation of p65 and IjBa and the level of PTEN while enhanced phosphorylation of PI3K and AKT. Importantly, emodin increased expression of miR-21 suppressed by LPS and miR-21 downregulation negated the protective functions of emodin. Conclusions: Emodin promoted cell growth presented by increasing viability and blocking apoptosis process with inflammation inhibition. The protective activity of emodin was mediated by miR-21 up-regulation.

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Section: Discussionmentioning

confidence: 99%

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Song

Cui

Zhao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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show abstract

“…Emodin has also been shown to inhibit the growth of Helicobacter pylori in vitro in a dose-dependent manner (13). Further in vitro experiments have demonstrated that emodin significantly inhibits the release of cytokines by mononuclear cells under lipopolysaccharide (LPS) stimulation, and also inhibits the endotoxin-induced secretion of tumor necrosis factor (TNF)-α, interleukin (IL)-1, IL-6, IL-8 and other inflammatory cytokines, thus affecting the immune activation associated with them (14,15).…”

Section: Introductionmentioning

confidence: 99%

Renoprotective effects of emodin against diabetic nephropathy in rat models are mediated via PI3K/Akt/GSK‑3β and Bax/caspase‑3 signaling pathways

2017

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Abstract. Emodin is the main active component of the Chinese medicine rhubarb, which has a variety of pharmacological effects and a high clinical value. Its anti-inflammatory and antitumor effects have been widely studied. The aim of the present study was to determine whether emodin has renoprotective effects, and to identify the potential underlying mechanisms in a rat model of diabetic nephropathy (DN). The changes in mean blood glucose levels, normalized kidney weight, urinary albumin excretion, serum creatinine levels and tubulointerstitial injury index (TII) scores of the rats with DN were significantly attenuated by emodin. Furthermore, treatment with emodin significantly inhibited inflammation-related factors and oxidative stress, suppressed the expression of intercellular adhesion molecule 1 (ICAM-1) and B-cell lymphoma 2-associated X protein (Bax), increased phosphorylated Akt and phosphorylated-glycogen synthase kinase 3 (p-GSK-3β) expression and inhibited caspase-3 activity in diabetic rats. These data suggest that emodin protects against DN and that the underlying mechanism may involve the suppression of inflammation, ICAM-1 and Bax, and activation of the PI3K/Akt/GSK-3β pathway.

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“…8 Otherwise, researches have put forward that emodin acted as an anti-inflammatory agent through a variety of signaling mechanisms. 9,10 Furthermore, a research pointed out that emodin restrained pneumonia via NF-κB pathway. 11 Although there is a lot of research on emodin, the intervention mechanism of emodin in inflammatory damage is not well understood until now.…”

mentioning

confidence: 99%

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

et al. 2020

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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

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Emodin suppresses LPS-induced inflammation in RAW264.7 cells through a PPARγ-dependent pathway

Cited by 106 publications

References 32 publications

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Emodin protects against lipopolysaccharide-induced inflammatory injury in HaCaT cells through upregulation of miR-21

Renoprotective effects of emodin against diabetic nephropathy in rat models are mediated via PI3K/Akt/GSK‑3β and Bax/caspase‑3 signaling pathways

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

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