Effects of neferine on TGF-β1 induced proliferation and gremlin expression in hepatic stellate cells

Li, Xiaofei; Lou, Lianqing; Wu, Shuang; Chen, Yongxin; Jin, Lingzhen

doi:10.3329/bjp.v7i3.11298

Cited by 3 publications

(4 citation statements)

References 10 publications

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“…The anti-proliferative effects of artesunate on smooth muscle cells were also demonstrated in vivo in a murine model of ovalbumin-induced allergic asthma 102 . In a rat hepatic stellate cell line, increasing artesunate concentration inhibited cellular proliferation as demonstrated by induction of a G0/G1 arrest 103 , and inhibition of proliferation in rat hepatic stellate cells was also described in other reports 104 , 105 . In a human hepatic stellate cell line, artesunate concentration-dependently reduced cellular viability via induction of apoptosis 106 .…”

Section: Cellular Effects Of Artemisinin Derivatives On Cells and Celsupporting

confidence: 57%

“…Artesunate also antagonized PDGF-BB-mediated activation of ERK and expression of cyclin D1, as well as AP-1 DNA-binding activity, suggesting that artesunate inhibits PDGF-BB-mediated stimulation of proliferation and collagen deposition through antagonism of ERK and of subsequent proliferative signaling through AP-1 and cyclin D1 104 . In another report using rat hepatic stellate cells, artesunate reduced cellular proliferation, reduced the quantity of collagen secreted, and upregulated MMP-13 expression 105 . Taken together, these reports collectively suggest that artemisinin drugs can robustly antagonize myofibroblast activation and downregulate expression of pro-fibrotic genes.…”

Section: Cellular Effects Of Artemisinin Derivatives On Cells and Celmentioning

confidence: 91%

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Artemisinin and artemisinin derivatives as anti-fibrotic therapeutics

Dolivo

Weathers

Dominko

2021

Acta Pharmaceutica Sinica B

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Fibrosis is a pathological reparative process that can occur in most organs and is responsible for nearly half of deaths in the developed world. Despite considerable research, few therapies have proven effective and been approved clinically for treatment of fibrosis. Artemisinin compounds are best known as antimalarial therapeutics, but they also demonstrate antiparasitic, antibacterial, anticancer, and anti-fibrotic effects. Here we summarize literature describing anti-fibrotic effects of artemisinin compounds in in vivo and in vitro models of tissue fibrosis, and we describe the likely mechanisms by which artemisinin compounds appear to inhibit cellular and tissue processes that lead to fibrosis. To consider alternative routes of administration of artemisinin for treatment of internal organ fibrosis, we also discuss the potential for more direct oral delivery of Artemisia plant material to enhance bioavailability and efficacy of artemisinin compared to administration of purified artemisinin drugs at comparable doses. It is our hope that greater understanding of the broad anti-fibrotic effects of artemisinin drugs will enable and promote their use as therapeutics for treatment of fibrotic diseases.

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Section: Cellular Effects Of Artemisinin Derivatives On Cells and Celsupporting

confidence: 57%

Section: Cellular Effects Of Artemisinin Derivatives On Cells and Celmentioning

confidence: 91%

Artemisinin and artemisinin derivatives as anti-fibrotic therapeutics

Dolivo

Weathers

Dominko

2021

Acta Pharmaceutica Sinica B

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“…HSC activation and imbalances in ECM metabolism and cytokines are key factors in the development of liver fibrosis (Page et al, ). Numerous therapeutic approaches have been assessed as antifibrotic therapies and include inhibiting HSCs (Li et al, ; Shah et al, ), antioxidants (Chowdhury et al, ; Huang et al, ), and inhibiting the secretion of ECM and cytokines (Li et al, ). However few drugs have emerged as an effective anti‐fibrotic strategy.…”

Section: Introductionmentioning

confidence: 99%

Herbal Formula, Baogan Yihao (BGYH), Prevented Dimethylnitrosamine(DMN)‐Induced Liver Injury in Rats

Liu

Shi

et al. 2017

Drug Development Research

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Preclinical Research Baogan Yihao (BGYH) is a traditional Chinese herbal medicine for the treatment of chronic liver diseases. In this study, the effects of BGYH on dimethylnitrosamine (DMN)-induced liver fibrosis were investigated using a rat model. BGYH alleviate liver damage, as indicated by decreased levels of AST, ALT, γ-GT, and AKP. BGYH also prevented collagen deposition and reduced pathological tissue injury in liver tissue. In fibrosis, high levels of α-SMA and TGF-β in liver tissue were markedly attenuated by BGYH. The inhibitory effect of BGYH on HSC-T6 proliferation demonstrated that BGYH exhibited significant hepatoprotective and antifibrogenic effects on DMN-induced liver injury. These findings suggest that BGYH may have therapeutic potential in the prevention and therapy of liver fibrosis. Drug Dev Res 78 : 155-163, 2017. © 2017 Wiley Periodicals, Inc.

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“…[18,19] The antifibrotic effect of neferine was reported in diabetic rats [20] and hepatic stellate cells. [21] However, there were no reports for the mechanistic action of neferine on cardiac fibrosis and hypertrophy-mediated cell death upon DOX administration. Therefore, the present study was designed to explore the protective action of neferine on Dox-induced fibrosis and hypertrophy in H9c2 cardiomyoblasts.…”

mentioning

confidence: 99%

Neferine attenuates doxorubicin‐induced fibrosis and hypertrophy in H9c2 cells

Lohanathan

Baskaran

Huang

et al. 2022

J Biochem & Molecular Tox

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Doxorubicin (DOX), an anthracycline antineoplastic candidate is used to treat various malignancies. Around 41% of patients undergoing DOX treatment develop acute cardiotoxicity. Preventing DOX‐induced cardiac fibrosis and hypertrophy helps in evading cardiac remodeling leading to cardiomyopathy and heart failure. Neferine, an alkaloid from the lotus has numerous pharmacological activities. The present study was designed to evaluate the protective effect of neferine on DOX‐mediated fibrosis and hypertrophy. DOX‐induced fibrosis involves activation of transforming growth factor‐β1 (TGF‐β1), matrix metalloproteinase 2 (MMP‐2), and MMP‐9 with concomitant downregulation of tissue inhibitors of MMPs (TIMP)‐1 and TIMP‐2 expressions in H9c2 cardiomyoblasts. Furthermore, DOX treatment also resulted in hypertrophy with the increased cell volume and overexpression of hypertrophy markers calcineurin, brain natriuretic peptide, and atrial natriuretic peptide. Finally, DOX treatment resulted in apoptosis through activation of p53. Pretreatment with neferine markedly activated SIRT1 expression and modulated the expression levels of TGF‐β1 and p53, thereby significantly reducing DOX‐induced fibrosis, hypertrophy, and apoptosis in H9c2 cardiomyoblasts.

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Effects of neferine on TGF-β1 induced proliferation and gremlin expression in hepatic stellate cells

Cited by 3 publications

References 10 publications

Artemisinin and artemisinin derivatives as anti-fibrotic therapeutics

Artemisinin and artemisinin derivatives as anti-fibrotic therapeutics

Herbal Formula, Baogan Yihao (BGYH), Prevented Dimethylnitrosamine(DMN)‐Induced Liver Injury in Rats

Neferine attenuates doxorubicin‐induced fibrosis and hypertrophy in H9c2 cells

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