In vitro anti-fibrotic activities of herbal compounds and herbs

Hu, Qin; Noor, Mazhar; Wong, Yuen Fei; Hylands, Peter J.; Simmonds, Monique S. J.; Xu, Qing; Jiang, Dan; Hendry, Bruce M.; Xu, Qihe

doi:10.1093/ndt/gfp245

Cited by 89 publications

(77 citation statements)

References 32 publications

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“…It reduces fibronectin expression by suppressing p38 signaling in diabetic rats and in high glucose-treated mesangial cells (4,21). Emodin also suppresses IL-1β-induced ECM production in mesangial cells (5) and inhibits collagen I expression in rat fibroblasts (22). However, its mechanisms are not fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Emodin inhibits extracellular matrix synthesis by suppressing p38 and ERK1/2 pathways in TGF-β1-stimulated NRK-49F cells

et al. 2011

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Abstract. emodin has been demonstrated to inhibit the fibrotic process in chronic renal disease, but its mechanisms have yet to be fully elucidated. This study was carried out to investigate the effects of emodin on extracellular matrix (ecM) synthesis in TGF-β1-stimulated NRK-49F cells. NRK-49F cells stimulated with TGF-β1 were incubated with various concentrations of emodin. ECM proteins, including collagen type III and fibronectin, were detected using ELISA. ERK1/2, p38 and JNK phosphorylation were measured by Western blotting. p38, ERK1/2 and JNK were respectively inhibited with the specific inhibitors SB203580, PD98059 and SP600125. Emodin slightly inhibited the expression of fibronectin and collagen type III in NRK-49F cells without TGF-β1 treatment, and significantly suppressed fibronectin and collagen type III secretion in TGF-β1-stimulated NRK-49F cells. ERK1/2 and p38 specific inhibitors, but not JNK inhibitor, suppressed the TGF-β1-induced expression of fibronectin and collagen type III. Our previous study demonstrated that there was no crosstalk between ERK1/2, p38 and JNK signals in TGF-β1-stimulated NRK-49F cells. Here, we found that emodin inhibited the phosphorylation of ERK1/2 and p38 significantly, but did not suppress the phosphorylation of JNK. In summary, emodin suppresses fibronectin and collagen type III expression via the inhibition of ERK1/2 and p38 phosphorylation in TGF-β1-stimulated NRK-49F cells.

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Section: Discussionmentioning

confidence: 99%

Emodin inhibits extracellular matrix synthesis by suppressing p38 and ERK1/2 pathways in TGF-β1-stimulated NRK-49F cells

et al. 2011

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“…Picrosirius red staining allows the collagen produced by cell cultures to be quantified (Hu et al, 2009;Xu et al, 2007). Exposure of HK-2 cells to 50 and 5 mg/ml AS for 48 h did not modify the amount of collagen produced as compared to the control condition ( Figure 6).…”

Section: Cispt-induced Collagen Deposition Is Limited By As Co-treatmentmentioning

confidence: 98%

“…Next, cells were washed with PBS, fixed with ice-cold methanol for 1 h at 4 C, rinsed twice with 1% acetic acid and stained for 2 h with 0.1% picrosirius red (PSR) staining solution (Hu et al, 2009). Wells were then rinsed three times with 1% acetic acid.…”

Section: Assessment Of Collagen Synthesismentioning

confidence: 99%

Potential nephroprotective effects of the Chinese herbAngelica sinensisagainst cisplatin tubulotoxicity

Bunel

Antoine

Nortier

et al. 2014

Pharmaceutical Biology

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Context: Acute kidney injury (AKI) is often encountered in patients receiving cisplatin (CisPt), a chemotherapeutic drug that induces numerous toxic side effects. Techniques used to limit nephrotoxicity during CisPt treatment are not fully effective; about a third of patients experience AKI. New nephroprotective strategies, including pharmacological approaches, must be developed. Objective: The present study investigated the nephroprotective potential of Angelica sinensis (Oliv.) Diels (Apiaceae) root towards CisPt tubulotoxicity. Materials and methods: HK-2 cells were incubated with CisPt (10 mM) and/or with a methanolic extract of A. sinensis (AS). Nephroprotective capacity was evaluated by means of cellular viability (resazurin assay) and apoptosis (annexin-V/PI staining), oxidative stress generation (H 2 DCF-DA oxidation), Ki-67 index (immunofluorescence), cell cycle analysis (DNA staining), cell migration rate (scratch assay), extracellular matrix deposition (collagen determination), and b-catenin relocalization. Results: CisPt decreased cell viability [76% versus Ctrl], which was associated with an increased apoptosis. Simultaneous treatment with 50 mg/ml AS enhanced cell survival [84% versus Ctrl] and decreased the apoptosis rate. AS could not alleviate CisPt-induced oxidative stress; but doses of 5 and 50 mg/ml raised the Ki-67 index [135 and 244% versus Ctrl] and cell migration rates [1.2 and 1.3-fold versus Ctrl]. Finally, both doses of AS limited the amount of collagen deposition [121.6 and 119.6% for 5 and 50 mg/ml, respectively, versus 131.0% for CisPt-treated cells] and prevented the relocalization of b-catenin from the membrane to the nucleus. Conclusion: These results confirm the nephroprotective potential of A. sinensis and require further investigations aiming at identifying its active compounds.

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“…In contrast to the lack of "anti-fibrotics" in Western medicine clinics, there is accumulating evidence suggesting anti-fibrotic effects of Chinese materia medicas (CMMs), i.e., medicinal materials used in traditional Chinese medicine (TCM) (Hu et al, 2007). However, most of these conclusions were drawn from animal models or patients and hence it was not clear whether the reported efficacy of those CMMs was secondary to inhibition of aetiological factors or inflammation, or whether they exerted genuine anti-fibrotic activities (Hu et al, 2009). We hypothesised that at least some of the "anti-fibrotic" herbal derivatives reported in the literature are indeed anti-fibrotic by antagonising TGF-1-specific pro-fibrotic pathways or common pathways of fibrosis.…”

Section: Introductionmentioning

confidence: 99%

“…We hypothesised that at least some of the "anti-fibrotic" herbal derivatives reported in the literature are indeed anti-fibrotic by antagonising TGF-1-specific pro-fibrotic pathways or common pathways of fibrosis. By employing the 2D in vitro model , we tested the anti-fibrotic activity of 21 CMM-derived compounds, 11 methanolic extracts of single CMMs and 27 formulae that contained two or more CMMs as mixtures, and found that five compounds, three single CMM extracts and 16 formulae had in vitro anti-fibrotic activities (Hu et al, 2009). Among the five CMM-derived compounds, three flavonoids (quercetin, baicalin and baicalein) showed similar dose-dependent in vitro antifibrotic activities while two non-flavonoids (salvianolic acid B and emodin) showed varied in vitro anti-fibrotic activities with poor dose dependency.…”

Section: Introductionmentioning

confidence: 99%

Knowledge-Based Discovery of Anti-Fibrotic and Pro-Fibrotic Activities from Chinese Materia Medica

Xu¹,

Wong²,

Qu³

et al. 2012

Recent Advances in Theories and Practice of Chinese Medicine

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In vitro anti-fibrotic activities of herbal compounds and herbs

Abstract: Five herbal compounds and three herbal extracts have in vitro anti-fibrotic activities. These data warrant further studies on these anti-fibrotic entities and suggest it a promising strategy to discover new anti-fibrotic drugs by screening more plant materials.

Cited by 89 publications

References 32 publications

Emodin inhibits extracellular matrix synthesis by suppressing p38 and ERK1/2 pathways in TGF-β1-stimulated NRK-49F cells

Emodin inhibits extracellular matrix synthesis by suppressing p38 and ERK1/2 pathways in TGF-β1-stimulated NRK-49F cells

Potential nephroprotective effects of the Chinese herbAngelica sinensisagainst cisplatin tubulotoxicity

Knowledge-Based Discovery of Anti-Fibrotic and Pro-Fibrotic Activities from Chinese Materia Medica

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