Emodin suppresses activation of hepatic stellate cells through <scp>p38</scp> mitogen‐activated protein kinase and <scp>Smad</scp> signaling pathways in vitro

Wang, Xiaoli; Niu, Chengu; Zhang, Xiaojie; Dong, Miaoxian

doi:10.1002/ptr.6182

Cited by 25 publications

(12 citation statements)

References 45 publications

(56 reference statements)

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“…43 Additionally, emodin relieved fibrosis symptoms via inactivation of TGFβ 1 -Smad signaling. 44 Our study was consistent with these results. Also, our study revealed that αSMA was notably activated in HK2 cells after TGFβ 1 treatment.…”

Section: Discussionsupporting

confidence: 93%

<p>Emodin Retarded Renal Fibrosis Through Regulating HGF and TGFβ–Smad Signaling Pathway</p>

Yang

Deng

et al. 2020

DDDT

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Background: Renal fibrosis is a frequently occurring type of chronic kidney disease that can cause end-stage renal disease. It has been verified that emodin or HGF can inhibit the development of renal fibrosis. However, the antifibrotic effect of emodin in combination with HGF remains unclear. Methods: Cell viability was detected with CCK8. Gene and protein expression in HK2 cells was detected by qRT-PCR and Western blot, respectively. Moreover, a unilateral ureteral obstruction-induced mouse model of renal fibrosis was established for investigating the antifibrotic effect of emodin in combination with HGF in vivo. Results: HGF notably increased the expression of collagen II in TGFβ-treated HK2 cells. In addition, HGF-induced increase in collagen II expression was further enhanced by emodin. In contrast, fibronectin, αSMA and Smad2 expression in TGFβ-stimulated HK2 cells was significantly inhibited by HGF and further decreased by combination treatment (emodin plus HGF). Moreover, we found that combination treatment exhibited better antifibrotic effects compared with emodin or HGF in vivo. Conclusion: These data demonstrated that emodin plus HGF exhibited better antifibrotic effects compared with emodin or HGF. As such, emodin in combination with HGF may serve as a new possibilty for treatment of renal fibrosis.

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Section: Discussionsupporting

confidence: 93%

<p>Emodin Retarded Renal Fibrosis Through Regulating HGF and TGFβ–Smad Signaling Pathway</p>

Yang

Deng

et al. 2020

DDDT

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“…Among them, the effect of Emo, Rhe, Alo, and Pru was particularly prominent. Interestingly, some previous studies have confirmed that Emo, Rhe, Alo, Chr, Phy, and Amy have shown different degrees of anti-liver fibrosis effects in in vivo and in vitro experiments (Woo et al 2002;Lian et al 2005;Lin et al 2008;Li et al 2016;Lian et al 2017;Wang et al 2018).…”

Section: Discussionmentioning

confidence: 91%

Hepatoprotective effect of Xiayuxue decoction ethyl acetate fraction against carbon tetrachloride-induced liver fibrosis in mice via inducing apoptosis and suppressing activation of hepatic stellate cells

Zhang

Zeng

et al. 2020

Pharmaceutical Biology

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“…The copyright holder for this preprint this version posted January 7, 2021. ; https://doi.org/10.1101/2021.01.07.425762 doi: bioRxiv preprint 1 4 TGF-β receptor engagement can also result in activation of several non-canonical signaling pathways including phosphatidylinositol-3-kinase (PI3K)/ Akt , mitogen activated protein kinases (MAPK) and Rho-like GTPases (Zhang, 2009;Yeganeh et al, 2013). Recent studies have demonstrated that treatment of a hepatic stellate cell line with emodin in vitro reduces constitutive activation of p38 MAPK, while having no effect on ERK 1/ 2 or JNK (Wang et al, 2018). These effects on p38 activity were independent of SMAD signaling.…”

Section: Discussionmentioning

confidence: 99%

Effects of Emodin, a Plant-Derived Anthraquinone, on TGF-β1-Induced Cardiac Fibroblast Activation and Function

Azhar

Carver

Fix

et al. 2021

Preprint

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Cardiac fibrosis accompanies a number of pathological conditions and results in altered myocardial structure, biomechanical properties and function. The signaling networks leading to fibrosis are complex, contributing to the general lack of progress in identifying effective therapeutic approaches to prevent or reverse this condition. Several studies have shown protective effects of emodin, a plant-derived anthraquinone, in animal models of fibrosis. A number of questions remain regarding the mechanisms whereby emodin impacts fibrosis. TGF-β1 is a potent stimulus of fibrosis and fibroblast activation. In the present study, experiments were performed to evaluate the effects of emodin on activation and function of cardiac fibroblasts following treatment with TGF-β1. We demonstrate that emodin attenuates TGF-β1-induced fibroblast activation and collagen accumulation in vitro. Emodin also inhibits activation of several canonical (SMAD2/3) and non-canonical (Erk1/2) TGF-β signaling pathways, while activating the p38 pathway. These results suggest that emodin may provide an effective therapeutic agent for fibrosis that functions via specific TGF-β signaling pathways.

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Emodin suppresses activation of hepatic stellate cells through p38 mitogen‐activated protein kinase and Smad signaling pathways in vitro

Cited by 25 publications

References 45 publications

<p>Emodin Retarded Renal Fibrosis Through Regulating HGF and TGFβ–Smad Signaling Pathway</p>

<p>Emodin Retarded Renal Fibrosis Through Regulating HGF and TGFβ–Smad Signaling Pathway</p>

Hepatoprotective effect of Xiayuxue decoction ethyl acetate fraction against carbon tetrachloride-induced liver fibrosis in mice via inducing apoptosis and suppressing activation of hepatic stellate cells

Effects of Emodin, a Plant-Derived Anthraquinone, on TGF-β1-Induced Cardiac Fibroblast Activation and Function

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