Potential therapeutic effects of a traditional Chinese formulation, BJ-JN, on liver fibrosis induced by carbon tetrachloride in rats

Zou, Yuhong; Yang, Yan; Li, Jun; Wu, Qing; Li, Weiping; J, Lu; Roberts, Michael S.

doi:10.1016/j.jep.2008.09.023

Cited by 19 publications

(14 citation statements)

References 26 publications

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“…Several drugs, including antisense TGF-β1 receptors, cytokines [24] , antioxidants, chemical drugs [25] , soluble type Ⅱ receptor of TGF-β1, and TGF-β1 antibodies [26] have been used in research work to block experimental hepatic fibrosis, but their effects were not as prosperous as we had expected. Some traditional Chinese drugs have been found effective in preventing fibrogenesis and other causes of chronic liver injury [27,28] , and this helps to develop a more hopeful future in controlling liver fibrosis and cirrhosis. Emodin is a main active monomer isolated from Giant Knotweed Rhizome, which is widely used in traditional Chinese herb treatment of liver cirrhosis [29] .…”

Section: Discussionmentioning

confidence: 99%

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Dong¹,

Yan²,

Zhang³

et al. 2009

WJG

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AIM: To investigate the role of emodin in protecting the liver against fibrogenesis caused by carbon tetrachloride (CCl4) in rats and to further explore the underlying mechanisms. METHODS:Rat models of experimental hepatic fibrosis were established by injection with CCl4; the treated rats received emodin via oral administration at a dosage of 20 mg/kg twice a week at the same time. Rats injected with olive oil served as a normal group. Histopathological changes were observed by hematoxylin and eosin staining. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum and hepatic hydroxyproline content were assayed by biochemical analyses. The mRNA and protein relevant to hepatic stellate cell (HSC) activation in the liver were assessed using real-time reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemistry, western blotting and enzymelinked immunosorbent assay. RESULTS:The degree of hepatic fibrosis increased markedly in the CCl4 group compared to the normal group (P < 0.01), and decreased markedly in the emodin group compared to the CCl4 group according to METAVIR scale (P < 0.01) compared with those in the normal control group (51.02 ± 10.64 IU/L and 132.28 ± 18.14 IU/L). The activities of serum ALT and AST were significantly higher in rats injected with CCl4 (289.25 ± 68.84 IU/L and 423.89 ± 35.67 IU/L, both P < 0.05).The activities of serum ALT and AST were significantly reduced by administration of emodin (176.34 ± 4 7. 2 9 I U / L a n d 2 2 6 . 1 ± 4 4. 5 2 I U / L , b o t h P < 0.05). Compared with the normal controls (54.53 ± 13.46 mg/g), hepatic hydroxyproline content was significantly higher in rats injected with CCl4 (120.27 ± 28.47 mg/g, P < 0.05). Hepatic hydroxyproline content was significantly reduced in the rats treated with emodin at 20 mg/kg (71.25 ± 17.02 mg/g, P < 0.05).Emodin significantly protected the liver from injury by reducing serum AST and ALT activities and reducing hepatic hydroxyproline content. The mRNA levels of transforming growth factor-β1 (TGF-β1), Smad4 and α-SMA in liver tissues were significantly down-regulated in SD rats that received emodin treatment. Furthermore, significant down-regulation of serum TGF-β1 protein levels and protein expression of Smad4 and α-SMA in liver tissues was also observed in the rats. Emodin inhibited HSC activation by reducing the abundance of TGF-β1 and Smad4. CONCLUSION:Emodin protects the rat liver from CCl4-induced fibrogenesis by inhibiting HSC activation. Emodin might be a therapeutic antifibrotic agent for the treatment of hepatic fibrosis.

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Section: Discussionmentioning

confidence: 99%

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Dong¹,

Yan²,

Zhang³

et al. 2009

WJG

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“…Liver fibrosis is characterized by altered hepatic function and the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases [1].…”

Section: Introductionmentioning

confidence: 99%

Effect of histidine on autotaxin activity in experimentally induced liver fibrosis

El-Batch

Ibrahim

Said

2010

J Biochem & Molecular Tox

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The aim of this study was to explain whether serum autotaxin (ATX) activity might be a target for regulation of liver fibrosis and to evaluate the hepatoprotective and antifibrotic effects of histidine in thioacetamide (TAA)-induced liver fibrosis in rats. This study was carried out on 100 Wistar Albino rats, classified into five groups, each containing 20 rats: Group I (control group), Group II: rats were given histidine intraperitoneally, Group III: rats were injected intraperitoneally with TAA, Group IV: rats were injected with L-histidine together with TAA, and Group V: rats were injected with TAA for 1 month then treated with intraperitoneal injection of L-histidine for another month. At the end of experiment, blood and liver were collected for determination of some liver enzymes, plasma total antioxidant capacity (TAC), serum ATX activity, and liver tissue hydroxyproline. Thioacetamide treatment caused significant increases in liver enzymes, ATX activities, and liver hydroxyproline, but a significant decrease in plasma's TAC. Upon treatment with histidine, a significant decrease in liver enzymes, ATX activities, and liver hydroxyproline was observed with a significant increase in plasma TAC in Group IV and a significant decrease in Group V. Histidine as an antioxidant has a protective effect on TAA-induced liver fibrosis; it is beneficial in rats not only by inhibition of collagen synthesis and increasing TAC but also by inhibition of ATX activities thus reducing its capacity to produce lysophosphatidic acid, which has a role in liver fibrosis. C 2010 Wiley Periodicals, Inc. J Biochem Mol Toxicol 25:143-150, 2011; View this article online at wileyonlinelibrary.com.

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“…The progression of liver fibrosis often develops into irreversible cirrhosis and is associated with liver cancer. [1][2][3] It is therefore imperative to reduce the damage to the liver and to slow down the progress of liver injury into fibrosis and cancer. Oxidative stress may be a common factor in chronic liver diseases of different etiologies.…”

Section: Introductionmentioning

confidence: 99%

MRI-based texture analysis: a potential technique to assess protectors against induced-liver fibrosis in rats

Mahmoud‐Ghoneim¹,

Amin²,

Corr³

2009

Radiology and Oncology

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Potential therapeutic effects of a traditional Chinese formulation, BJ-JN, on liver fibrosis induced by carbon tetrachloride in rats

Cited by 19 publications

References 26 publications

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Effect of histidine on autotaxin activity in experimentally induced liver fibrosis

MRI-based texture analysis: a potential technique to assess protectors against induced-liver fibrosis in rats

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Potential therapeutic effects of a traditional Chinese formulation, BJ-JN, on liver fibrosis induced by carbon tetrachloride in rats

Cited by 19 publications

References 26 publications

Emodin protects rat liver from CCl4-induced fibrogenesis via inhibition of hepatic stellate cells activation

Emodin protects rat liver from CCl4-induced fibrogenesis via inhibition of hepatic stellate cells activation

Effect of histidine on autotaxin activity in experimentally induced liver fibrosis

MRI-based texture analysis: a potential technique to assess protectors against induced-liver fibrosis in rats

Contact Info

Product

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Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation

Emodin protects rat liver from CCl₄-induced fibrogenesis via inhibition of hepatic stellate cells activation