Antifibrotic effects of a herbal combination regimen on hepatic fibrotic rats

Lin, Yun‐Lian; Hsu, Yi‐Chao; Chiu, Yung-Tsung; Huang, Yi-Tsau

doi:10.1002/ptr.2265

Cited by 27 publications

(14 citation statements)

References 40 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These data suggest that secreted bioactive TGF-β1 is regulated by host proteins furin and TSP-1, and bioactive TGF-β1 plays an important role in the activation of HSCs. Our data is in agreement with previously published work on TGF-β1 stimulation of HSCs and elucidates the role of secreted TGF-β1 from HCV-infected cells [61], [62], [63], [64]. Another hallmark of HSC activation is an invasive phenotype [64].…”

Section: Discussionsupporting

confidence: 93%

Activation of TGF-β1 Promoter by Hepatitis C Virus-Induced AP-1 and Sp1: Role of TGF-β1 in Hepatic Stellate Cell Activation and Invasion

2013

View full text Add to dashboard Cite

Our previous studies have shown the induction and maturation of transforming growth factor-beta 1 (TGF-β1) in HCV-infected human hepatoma cells. In this study, we have investigated the molecular mechanism of TGF-β1 gene expression in response to HCV infection. We demonstrate that HCV-induced transcription factors AP-1, Sp1, NF-κB and STAT-3 are involved in TGF-β1 gene expression. Using chromatin immunoprecipitation (ChIP) assay, we further show that AP-1 and Sp1 interact with TGF-b1 promoter in vivo in HCV-infected cells. In addition, we demonstrate that HCV-induced TGF-β1 gene expression is mediated by the activation of cellular kinases such as p38 MAPK, Src, JNK, and MEK1/2. Next, we determined the role of secreted bioactive TGF-β1 in human hepatic stellate cells (HSCs) activation and invasion. Using siRNA approach, we show that HCV-induced bioactive TGF-β1 is critical for the induction of alpha smooth muscle actin (α-SMA) and type 1 collagen, the markers of HSCs activation and proliferation. We further demonstrate the potential role of HCV-induced bioactive TGF-β1 in HSCs invasion/cell migration using a transwell Boyden chamber. Our results also suggest the role of HCV-induced TGF-β1 in HCV replication and release. Collectively, these observations provide insight into the mechanism of TGF-β1 promoter activation, as well as HSCs activation and invasion, which likely manifests in liver fibrosis associated with HCV infection.

show abstract

Section: Discussionsupporting

confidence: 93%

Activation of TGF-β1 Promoter by Hepatitis C Virus-Induced AP-1 and Sp1: Role of TGF-β1 in Hepatic Stellate Cell Activation and Invasion

2013

View full text Add to dashboard Cite

show abstract

“…Two phthalides, Z,Z '-6,8' ,7,3'-diligustilide (1) and levistolide A (2) from LC significantly abrogate PDGF-BB-induced proliferation in both rats and human HSC lines, which is related to inhibition of cell cycle and induction of apoptosis. They might be potential antifibrotic drugs for the treatment and prevention of hepatic fibrosis (Lin et al, 2006(Lin et al, , 2008Lee et al, 2007).…”

Section: Antifibrotic Effectsmentioning

confidence: 99%

Ligusticum chuanxiongHort: A review of chemistry and pharmacology

Ran¹,

Ma²,

Peng³

et al. 2011

Pharmaceutical Biology

160

View full text Add to dashboard Cite

A large number of pharmacological and chemical studies during the last 10 years have demonstrated the vast medicinal potential of LC. It is still very clear that LC is a plant with widespread use now and also with extraordinary potential for the future. The documents strongly support the view that LC has beneficial therapeutic properties and indicates its potential as an effective adaptogenic herbal remedy.

show abstract

“…The response on immune system could be attributed to its action on T lymphocytes (Gharagozloo et al 2010;Johnson et al 2003). Although silymarin mechanisms were not completely clarified, their anti-inflammatory activity could be at least partially attributed to its inhibitor role on pleiotropic NF-kB (Lin et al 2008) and on reduction of TNF, IL-1α, IL-6 (Agarwal 2000), and IL-2 and IL-4 .…”

Section: Introductionmentioning

confidence: 99%

Silymarin treatment reduces granuloma and hepatic fibrosis in experimental schistosomiasis

et al. 2010

View full text Add to dashboard Cite

The schistosomiasis is a parasitic infection with relevant social impact and an important health problem in many countries around world. The pathology of this infection is characterized by a granulomatous reaction around parasite eggs and by hepatic fibrosis. Silymarin, a complex compound isolated from Silybum marianum (L.) Gaertner, have been described as hepatoprotective, antioxidant, antifibrotic, immunomodulator, and anti-neoplastic agent. Some of these capacities could potentially protect against pathology in schistosomiasis. Herein, we evaluated the effects of silymarin on parasite burden, granuloma sizes, and liver fibrosis, which are associated with severity and morbidity of this disease. BALB/c mice treated intraperitoneally with 10, 20, or 25 doses of silymarin (10 mg kg(-1)) suspended in carboxymethylcellulose were analyzed at 55 days post-infection. Silymarin (1) did not affect parasite oviposition capacity; (2) reduced granulomatous peri-ovular reaction in the liver, and (3) decreased hepatic fibrosis in this infection. Taken together, these data suggest that treatment with silymarin at acute phase of schistosomiasis may result in a mild course of murine schistosomiasis and can be a promising complementary treatment reverting sequelae of this infection.

show abstract

Antifibrotic effects of a herbal combination regimen on hepatic fibrotic rats

Cited by 27 publications

References 40 publications

Activation of TGF-β1 Promoter by Hepatitis C Virus-Induced AP-1 and Sp1: Role of TGF-β1 in Hepatic Stellate Cell Activation and Invasion

Activation of TGF-β1 Promoter by Hepatitis C Virus-Induced AP-1 and Sp1: Role of TGF-β1 in Hepatic Stellate Cell Activation and Invasion

Ligusticum chuanxiongHort: A review of chemistry and pharmacology

Silymarin treatment reduces granuloma and hepatic fibrosis in experimental schistosomiasis

Contact Info

Product

Resources

About