Polyprenols from Taxus chinensis var. mairei prevent the development of CCl4-induced liver fibrosis in rats

Yu, Jianchun; Wang, Yanbin; Hua, Qian; Zhao, Yunpeng; Liu, Bentong; Fu, Chengxin

doi:10.1016/j.jep.2012.04.030

Cited by 29 publications

(21 citation statements)

References 43 publications

(43 reference statements)

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“…29 TGF-b is downregulated in animal models of fibrosis by treatment with curcumin, 30 epigallocatechin-3-gallate, 6 or polyprenols. 7 Present data confirm that melatonin also decreases TGF-b expression in CCl 4 -treated mice, a fact that undoubtedly contributes to the interference of the indol with the activation of HSCs. TGF-b signals stimulate through transmembrane receptors cytoplasmic Smad proteins, which in turn modulate the transcription of target genes, including those encoding ECM components.…”

Section: Discussionsupporting

confidence: 81%

“…38 The expression of amphiregulin increases markedly in liver injury induced by CCl 4 , 39 and amphiregulin deficient-mice develop significantly less collagen accumulation. 40 We have previously reported that suppression of amphiregulin signals contributes to the protective effects of quercetin in cirrhotic rats with common bile duct ligation, 7 and in mice fed a methionine-choline-deficient diet. 2 It is also known that amphiregulin amplifies the HSC response through increased production of CTGF and TIMP-1.…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress aggravates liver fibrosis. 5 Thus, inhibiting oxidative stress has been considered a potential useful strategy to prevent the development of hepatic fibrogenesis, and it has been reported that antioxidants such as epigallocatechin-3-gallate, 6 polyprenols, 7 quercetin, 8 or proanthocyanidin, 9 among others, may prevent liver injury in different animal models of fibrosis.…”

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confidence: 99%

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Melatonin limits the expression of profibrogenic genes and ameliorates the progression of hepatic fibrosis in mice

Crespo

San‐Miguel

Fernández

et al. 2015

Translational Research

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We investigated whether melatonin ameliorates fibrosis and limits the expression of fibrogenic genes in mice treated with carbon tetrachloride (CCl 4 ). Mice in treatment groups received CCl 4 5 mL/g body weight intraperitoneally twice a week for 4 or 6 weeks. Melatonin was given at 5 or 10 mg/kg/d intraperitoneally, beginning 2 weeks after the start of CCl 4 administration. Treatment with CCl 4 resulted in fibrosis evidenced by the staining of Van Gieson and a-smooth muscle actin (a-SMA) positive cells in the liver. At both 4 and 6 weeks, CCl 4 induced an increase in the messenger RNA levels of collagens I and III, transforming growth factor (TGF)-b, platelet-derived growth factor (PDGF), connective tissue growth factor (CTGF), amphiregulin, matrix metalloproteinase (MMP)-9, and tissue inhibitor of metalloproteinase (TIMP)-1. Protein concentrations of CTGF, amphiregulin, MMP-9, TIMP-1, and phospho-Smad3 were also significantly augmented in fibrotic mice. Melatonin successfully attenuated liver injury, as shown by histopathology and decreased levels of serum transaminases. Immunohistochemical staining of a-SMA indicated an abrogation of hepatic stellate cell activation by the indol. Furthermore, melatonin treatment resulted in significant inhibition of the expression of collagens I and III, TGF-b, PDGF, CTGF, amphiregulin, and phospho-Smad3. The MMP-9 activity decreased and the expression of nuclear factor erythroid-2-related factor 2 (Nrf2) increased in mice receiving melatonin. Data obtained suggest that attenuation of multiple profibrogenic gene pathways contributes to the beneficial effects of melatonin in mice with CCl 4 -induced liver fibrosis. (Translational Research 2015;165:346-357) Abbreviations: a-SMA ¼ a-smooth muscle actin; CCl 4 ¼ carbon tetrachloride; CTGF ¼ connective tissue growth factor; HSC ¼ hepatic stellate cell; MMP-9 ¼ matrix metalloproteinase 9; Nrf2 ¼ nuclear factor erythroid 2-related factor 2; PDGF ¼ platelet-derived growth factor; TGF-b ¼ transforming growth factor b; TIMP-1 ¼ tissue inhibitor of metalloproteinase 1 H epatic fibrosis is a reversible wound-healing response to either acute or chronic cellular injury from a wide variety of etiologies, characterized by an excessive deposition of extracellular matrix (ECM) resulting in liver dysfunction and irreversible cirrhosis. During liver fibrogenesis, hepatic stellate cells (HSCs) undergo activation to a a-smooth muscle actin (SMA)-positive myofibroblastic phenotype and synthesize excess ECM components, particularly collagen. 1 Among the numerous From the

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Melatonin limits the expression of profibrogenic genes and ameliorates the progression of hepatic fibrosis in mice

Crespo

San‐Miguel

Fernández

et al. 2015

Translational Research

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“…The cDNA PCR amplification conditions were as follows: initial denaturation at 95 C for 5 s followed by 40 cycles of denaturation at 95 C for 5 s and annealing at 60 C for 20 s. Gene expression levels were normalized to GAPDH mRNA. Fluorescence data from each sample were analyzed by the 2 ÀDDCt method (Yu et al, 2012).…”

Section: Total Rna Extraction and Real-time (Rt)-pcrmentioning

confidence: 99%

“…Previous studies have demonstrated that many natural compounds derived from herbs can reduce the severity of hepatic fibrosis in vivo and in vitro (Lee et al, 2012;Wang et al, 2010;Yu et al, 2012). Hydroxysafflor yellow A (HSYA) is an active ingredient of the herb Carthamus tinctorius L. (Asteraceae) (safflower) (Sun et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Hydroxysafflor yellow A suppresses liver fibrosis induced by carbon tetrachloride with high-fat diet by regulating PPAR-γ/p38 MAPK signaling

Liu

Wang

Liu

et al. 2014

Pharmaceutical Biology

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Context: One approach to protect against liver fibrosis is the use of herb-derived natural compounds, such as hydroxysafflor yellow A (HSYA). The antifibrosis effect of HYSA against liver fibrosis has been investigated; however, its mechanisms have not yet been entirely revealed. Objectives: To study the protective effects of HSYA on liver fibrosis induced by carbon tetrachloride (CCl 4 ) and a high-fat diet (HFD), and to determine the mechanism of action of HSYA. Materials and methods: CCl 4 and HFD were used to mimic liver fibrosis in rats, and serum biochemical indicators were determined. The antifibrosis effects of HSYA were evaluated and its mechanisms were investigated by histopathological analysis, immunohistochemical staining, enzyme-linked immunosorbent assays, real-time-PCR, and western blotting. Results: HSYA reduced CCl 4 -and HFD-mediated liver fibrosis and ameliorated serum biochemical indicator, downregulated the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1) (0.31 ± 0.03 protein, 0.59 ± 0.02 mRNA) and transformin growth factor-b1 (TGF-b1) (0.81 ± 0.02 protein, 0.58 ± 0.04 mRNA), and upregulated the expression of peroxisome proliferator-activated receptor-g (PPAR-g) (1.57 ± 0.13 protein, 2.48 ± 0.19 mRNA) and matrix metallopeptidases-2 (MMP-2) (2.31 ± 0.16 protein, 2.79 ± 0.22 mRNA) (p50.01, versus model group). These effects were significantly attenuated by PPAR-g antagonist GW9662 via blocking the phosphorylation of p38 MAPK. Discussion and conclusion: These data demonstrate a novel role for HSYA in inhibiting CCl 4 -and HFD-mediated liver fibrosis, and reveal that PPAR-g and p38 MAPK signaling play pivotal roles in the prevention of liver fibrosis induced by CCl 4 and HFD.

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Plant polyprenols reduce demyelination and recover impaired oligodendrogenesis and neurogenesis in the cuprizone murine model of multiple sclerosis

Khodanovich

Pishchelko

Glazacheva

et al. 2019

Phytotherapy Research

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Recent studies showed hepatoprotective, neuroprotective, and immunomodulatory properties of polyprenols isolated from the green verdure of Picea abies (L.) Karst . This study aimed to investigate effects of polyprenols on oligodendrogenesis, neurogenesis, and myelin content in the cuprizone demyelination model. Demyelination was induced by 0.5% cuprizone in CD‐1 mice during 10 weeks. Nine cuprizone‐treated animals received daily injections of polyprenols intraperitoneally at a dose of 12‐mg/kg body weight during Weeks 6–10. Nine control animals and other nine cuprizone‐treated received sham oil injections. At Week 10, brain sections were stained for myelin basic protein, neuro‐glial antigen‐2, and doublecortin to evaluate demyelination, oligodendrogenesis, and neurogenesis. Cuprizone administration caused a decrease in myelin basic protein in the corpus callosum, cortex, hippocampus, and the caudate putamen compared with the controls. Oligodendrogenesis was increased, and neurogenesis in the subventricular zone and the dentate gyrus of the hippocampus was decreased in the cuprizone‐treated group compared with the controls. Mice treated with cuprizone and polyprenols did not show significant demyelination and differences in oligodendrogenesis and neurogenesis as compared with the controls. Our results suggest that polyprenols can halt demyelination, restore impaired neurogenesis, and mitigate reactive overproduction of oligodendrocytes caused by cuprizone neurotoxicity.

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Polyprenols from Taxus chinensis var. mairei prevent the development of CCl4-induced liver fibrosis in rats

Cited by 29 publications

References 43 publications

Melatonin limits the expression of profibrogenic genes and ameliorates the progression of hepatic fibrosis in mice

Melatonin limits the expression of profibrogenic genes and ameliorates the progression of hepatic fibrosis in mice

Hydroxysafflor yellow A suppresses liver fibrosis induced by carbon tetrachloride with high-fat diet by regulating PPAR-γ/p38 MAPK signaling

Plant polyprenols reduce demyelination and recover impaired oligodendrogenesis and neurogenesis in the cuprizone murine model of multiple sclerosis

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