Curcumin Ameliorates Renal Fibrosis by Inhibiting Local Fibroblast Proliferation and Extracellular Matrix Deposition

Zhou, Xiangjun; Zhang, Jie; Xu, Changgeng; Wang, Wei

doi:10.1254/jphs.14173fp

Cited by 57 publications

(50 citation statements)

References 23 publications

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“…Immunohistochemistry was performed as described previously (Zhou et al . ). Slides were deparaffinized in xylene and hydrated in a graded ethanol series.…”

Section: Methodsmentioning

confidence: 97%

Membrane rafts–redox signalling pathway contributes to renal fibrosis via modulation of the renal tubular epithelial–mesenchymal transition

Han

Tang

et al. 2018

The Journal of Physiology

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The membrane rafts (MRs)-redox pathway is characterized by NADPH oxidase subunit clustering and activation through lysosome fusion, V-type proton ATPase subunit E2 (encoded by the Atp6v1e2 gene) translocation and sphingomyelin phosphodiesterase 1 (SMPD1, encoded by the SMPD1 gene) activation. In the present study, we hypothesized that the MRs-redox-derived reactive oxygen species (ROS) are involved in renal inflammation and fibrosis by promoting renal tubular epithelial-mesenchymal transition (EMT). Results show that transforming growth factor-β1 (TGF-β1) acutely induced MR formation and ROS production in NRK-52E cells, a rat renal tubular cell line. In addition, transfection of Atp6v1e2 small hairpin RNAs (shRNA) and SMPD1 shRNA attenuated TGF-β1-induced changes in EMT markers, including E-cadherin, α-smooth muscle actin (α-SMA) and fibroblast-specific protein-1 (FSP-1) in NRK-52E cells. Moreover, Erk1/2 activation may be a downstream regulator of the MRs-redox-derived ROS, because both shRNAs significantly inhibited TGF-β1-induced Erk1/2 phosphorylation. Further in vivo study shows that the renal tubular the MRs-redox signalling pathway was activated in angiotensin II (AngII)-induced hypertension, as indicated by the increased NADPH oxidase subunit Nox4 fraction in the MR domain, SMPD1 activation and increased ROS content in isolated renal tubular cells. Finally, renal transfection of Atp6v1e2 shRNA and SMPD1 shRNA significantly prevented renal fibrosis and inflammation, as indicated by the decrease of α-SMA, fibronectin, collagen I, monocyte chemoattractant protein-1 (MCP-1), intercellular cell adhesion molecule-1 (ICAM-1) and tumour necrosis factor-α (TNF-α) in kidneys from AngII-infused rats. It was concluded that the the MRs-redox signalling pathway is involved in TGF-β1-induced renal tubular EMT and renal inflammation/fibrosis in AngII-induced hypertension.

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“…Immunohistochemistry was performed as described previously (Zhou et al . ). Slides were deparaffinized in xylene and hydrated in a graded ethanol series.…”

Section: Methodsmentioning

confidence: 97%

Membrane rafts–redox signalling pathway contributes to renal fibrosis via modulation of the renal tubular epithelial–mesenchymal transition

Han

Tang

et al. 2018

The Journal of Physiology

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“…Curcumin treatment inhibited TGF- β 1mRNA expression [19]. And this inhibitory effect was mediated through reducing the phosphorylation of Smad2 and Smad3 [27]. In addition, pretreatment of curcumin resisted renal fibrosis by downregulating TGF- β 1 receptor II in TGF- β 1 stimulated NRK49F rat renal fibroblasts [57].…”

Section: Curcumin Is Also Actively Involved In Activation Stage Ofmentioning

confidence: 99%

“…In UUO mice, curcumin treatment (50 mg/kg and 100 mg/kg for 14 days, oral gavage) increased PPAR- γ expression and decreased phosphorylated Smad 2/3 [27]. This was also reflected in TGF- β 1 stimulated proximal tubular epithelial cell HK-2 cells [50] and 5/6 Nx rats [16].…”

Section: Curcumin Is Also Actively Involved In Activation Stage Ofmentioning

confidence: 99%

Recent Advances of Curcumin in the Prevention and Treatment of Renal Fibrosis

Sun

Liu

et al. 2017

BioMed Research International

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Curcumin, a polyphenol derived from the turmeric, has received attention as a potential treatment for renal fibrosis primarily because it is a relatively safe and inexpensive compound that contributes to kidney health. Here, we review the literatures on the applications of curcumin in resolving renal fibrosis in animal models and summarize the mechanisms of curcumin and its analogs (C66 and (1E,4E)-1,5-bis(2-bromophenyl) penta-1,4-dien-3-one(B06)) in preventing inflammatory molecules release and reducing the deposition of extracellular matrix at the priming and activation stage of renal fibrosis in animal models by consulting PubMed and Cnki databases over the past 15 years. Curcumin exerts antifibrotic effect through reducing inflammation related factors (MCP-1, NF-κB, TNF-α, IL-1β, COX-2, and cav-1) and inducing the expression of anti-inflammation factors (HO-1, M6PRBP1, and NEDD4) as well as targeting TGF-β/Smads, MAPK/ERK, and PPAR-γ pathways in animal models. As a food derived compound, curcumin is becoming a promising drug candidate for improving renal health.

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“…In various animal models of acute and chronic kidney injury, curcumin treatment has been shown to mitigate renal injury (59–61), possibly by reduced activation of the pro-inflammatory transcription factor NFκB and its downstream target tumor necrosis factor-α (TNF-α), concomitant with an increase in the anti-inflammatory transcription factor peroxisome proliferator-activated receptor-γ (PPARγ) (62, 63). Curcumin has been shown to slow cyst growth in vitro in a dose-response manner, using both the Madin–Darby canine kidney cell cyst model and an embryonic kidney cyst model (64).…”

Section: Clinical Trials In Adults With Adpkd and Implications For Pementioning

confidence: 99%

Clinical Trials in Pediatric Autosomal Dominant Polycystic Kidney Disease

Cadnapaphornchai

2017

Front. Pediatr.

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Autosomal dominant polycystic kidney disease (ADPKD) is the most common hereditary kidney disease and is associated with concerning long-term implications for kidney function and cardiovascular health. Early intervention is needed in order to mitigate these long-term complications. Herein, we review important findings from recent clinical trials in ADPKD and their relevance to affected children and young adults and consider future directions for intervention. Recent clinical trials support aggressive control of blood pressure with blockade of the renin-angiotensin-aldosterone system as well as potential benefit of pravastatin therapy in children and young adults with ADPKD. There are several other candidate therapies, some of which have shown benefit in adult ADPKD, which require further investigation in affected children.

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Curcumin Ameliorates Renal Fibrosis by Inhibiting Local Fibroblast Proliferation and Extracellular Matrix Deposition

Cited by 57 publications

References 23 publications

Membrane rafts–redox signalling pathway contributes to renal fibrosis via modulation of the renal tubular epithelial–mesenchymal transition

Membrane rafts–redox signalling pathway contributes to renal fibrosis via modulation of the renal tubular epithelial–mesenchymal transition

Recent Advances of Curcumin in the Prevention and Treatment of Renal Fibrosis

Clinical Trials in Pediatric Autosomal Dominant Polycystic Kidney Disease

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