Traditional Chinese Medicine (TCM) for fibrotic liver disease: Hope and hype

Zhang, Lijun; Schuppan, Detlef

doi:10.1016/j.jhep.2014.03.009

Cited by 81 publications

(56 citation statements)

References 9 publications

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“…Although hepatic fibrosis is reversible when the causative etiology is removed, the etiology could not be eradicated (Bissell, ; Fagone et al, ; Y. Zhu et al, ). Alternative and/or specific antifibrotic therapies are needed in part because of the recognized multifactorial etiology of hepatic fibrosis (reviewed by L. Zhang & Schuppan, ). The discovery of novel mechanisms of action is a necessary task for pharmacotherapy for hepatic fibrosis (reviewed by Rotman & Sanyal, ).…”

Section: Discussionmentioning

confidence: 99%

Emodin suppresses activation of hepatic stellate cells through p38 mitogen‐activated protein kinase and Smad signaling pathways in vitro

Wang

Niu

Zhang

et al. 2018

Phytotherapy Research

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The aim of this study was to evaluate the hypothesis that emodin inhibits extracellular matrix (ECM)-related gene expression in activated hepatic stellate cells (HSCs) by blocking canonical or/and noncanonical components of transforming growth factor β1 (TGFβ1) intracellular signaling. Here, we demonstrate that emodin suppressed the gene expression of HSCs activation markers type I collagen, fibronectin, and α-smooth muscle actin, as well as HSCs proliferation. Mechanistically, emodin suppresses TGFβ1, TGFβ receptor II, TGFβ receptor I, and Smad4 gene expression, as well as Smad luciferase activity. Simultaneously, emodin reduced p38 mitogen-activated protein kinase (p38 ) activity but not c-Jun N-terminal kinases and extracellular signal-regulated kinases 1 and 2 phosphorylation in HSC-T6 cells. Interestingly, deprivation of TGFβ using a neutralizing antibody abolished emodin-mediated inhibitions of the both Smad transcriptional activity and p38 phosphorylation. Furthermore, emodin-mediated inhibition of HSCs activation could be partially blocked by PD98059 inhibition of p38 or short hairpin RNA-imposed knockdown of Smad4. Conversely, simultaneous inhibition of Smad4 and p38 pathways completely reverses the effects of emodin, suggesting that Smad and p38 locate downstream of TGFβ1 and regulate collagen genes expression in HSCs. Collectively, these data suggest that emodin is a promising candidate for the treatment of hepatic fibrosis.

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Section: Discussionmentioning

confidence: 99%

Emodin suppresses activation of hepatic stellate cells through p38 mitogen‐activated protein kinase and Smad signaling pathways in vitro

Wang

Niu

Zhang

et al. 2018

Phytotherapy Research

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“…With the continuous deepening of theoretical research and clinical research of Chinese medicine, as one of the drug treatment pathways of NAFLD, traditional Chinese medicine has certain advantages in the prevention and treatment of NAFLD [27,28]. Previously, many Chinese decoctions, including Gegen Qinlian decoction [29], Yinchenhao decoction [30], Hua Tan Qu Shi decoction [31], Lingguizhugan decoction [32], and Qushi Huayu decoction [33], have been demonstrated to be effective in the treatment of NAFLD.…”

Section: Discussionmentioning

confidence: 99%

Cangju Qinggan Jiangzhi Decoction Reduces the Development of NonAlcoholic Steatohepatitis and Activation of Kupffer Cells

Cheng

Chen

Jian

et al. 2018

Cell Physiol Biochem

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Background/Aims: Nonalcoholic steatohepatitis (NASH) is defined as lipid accumulation with hepatic injury, inflammation and early to moderate fibrosis. Kupffer cells play a crucial role in promoting hepatic inflammation, which further facilitates the development of NASH. Here we investigated the effects of Cangju Qinggan Jiangzhi decoction (CQJD) on high fat diet (HFD) and methionine-choline deficient (MCD) induced mouse NASH pathogenesis. Methods: Mouse NASH models were developed by HFD and MCD diet. The treated mice were divided into three groups: the control group (n = 10), the low-dose CQJD treatment group (n = 10) and the high-dose CQJD treatment group (n = 10). The hepatic injury, inflammation, and apoptotic molecules were evaluated by H&E staining, immunohistochemistry and real-time PCR. Kupffer cells were isolated from control mice and CQJD-treated mice after stimulation by lipopolysaccharide (LPS) and/or palmitic acid. The level of the inflammatory cytokines TNFα, IL1β, and CCL2 was measured by ELISA. Results: The HFD-fed mice displayed significant metabolic, inflammatory, and oxidative stress-related alterations due to hepatic lipid accumulation. CQJD treatment largely normalized the hepatic injury, lowered the ALT/AST level, and reduced the severity of liver inflammation, as revealed by the decreased inflammatory cytokines levels. In vitro, CQJD blocked the activation of LPS- or palmitic acid-primed Kupffer cells in a dose-dependent manner. In the MCD diet-induced NASH mice, similar therapeutic effects of CQJD were also observed. Conclusion: CQJD ameliorates mouse nonalcoholic steatohepatitis. The reduction in liver injury and inflammation induced by CQJD is associated with reduced activation of Kupffer cells. Our results suggest that CQJD is a promising therapeutic strategy in clinical steatohepatitis.

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“…The onset of sickness is considered as the imbalance of Yin and Yang, leading to miscellaneous symptoms in the course of disease. 73 Herbal physicians treat patients as a whole and prescribe individual formulas based on the different body habitus. However, in the clinical trials, the interventions for all the patients recruited are the same, regardless of the different body habitus, contradicting the therapeutic pillars of Chinese herbalism.…”

Section: Current Critical Issues and Hurdles And Future Perspectivesmentioning

confidence: 99%

Herbal Medicines for Hepatitis C Virus Infection: The Exploratory Journey from Bench to Bedside Still Has a Long Way to Go

Xiao-ya¹,

Zhang²,

Xie³

et al. 2019

Journal of Exploratory Research in Pharmacology

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Hepatitis C virus (HCV) infects at least 150 million people chronically worldwide. It is a major risk factor for cirrhosis, hepatocellular carcinoma, and death. Direct-acting antiviral therapy is very efficacious in treating HCV infection but it is inaccessible and unavailable in some developing countries. Therefore, searching for more effective and easily accessible regimens remains an urgent need. The aim of this article is to review the anti-HCV effects of herbal medicines from experimental to clinical evidence, and discuss current issues, hurdles and future perspectives for their application from bench to bedside. Numerous in vitro studies have indicated that many herbs work effectively in exerting anti-HCV activities. Yet, only a few animal experiments have been conducted that demonstrate the anti-HCV effects of these medicines; in addition, these results do not show an ability to eliminate the virus completely from the infected animals. Thus far, clinical trials have produced inconclusive anti-HCV results in terms of efficacy and safety, presumably due to the lack of the quality of methodologies used in the trials. In conclusion, despite apparent anti-HCV activities in vitro, clinical efficacy and safety of herbal medicines for the treatment of HCV infection have not been revealed convincingly. More animal studies using ideal models and more well-designed clinical trials with a larger sample sizes and longer treatment periods, taking the body habitus into consideration, are required to further assess the efficacy and safety of herbal medicines for HCV infection.

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Traditional Chinese Medicine (TCM) for fibrotic liver disease: Hope and hype

Cited by 81 publications

References 9 publications

Emodin suppresses activation of hepatic stellate cells through p38 mitogen‐activated protein kinase and Smad signaling pathways in vitro

Emodin suppresses activation of hepatic stellate cells through p38 mitogen‐activated protein kinase and Smad signaling pathways in vitro

Cangju Qinggan Jiangzhi Decoction Reduces the Development of NonAlcoholic Steatohepatitis and Activation of Kupffer Cells

Herbal Medicines for Hepatitis C Virus Infection: The Exploratory Journey from Bench to Bedside Still Has a Long Way to Go

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