Crocin attenuates CCl<sub>4</sub>-induced liver fibrosis via PPAR-γ mediated modulation of inflammation and fibrogenesis in rats

Chhimwal, Jyoti; Sharma, Supriya; Kulurkar, Pankaj Markand; Patial, Vikram

doi:10.1177/0960327120937048

Cited by 37 publications

(24 citation statements)

References 36 publications

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“…showed that crocin decreased the hepatic fibrosis via expression of peroxisome proliferator-activated receptor γ (PPAR-γ), modulating the inflammatory and fibrogenic pathways. 83 These results are consistent with another study showing the anti-fibrotic and anti-inflammatory properties of crocin in thioacetamide (TAA)-induced liver fibrosis. 47 …”

Section: Discussionsupporting

confidence: 92%

Therapeutic potential of active components of saffron in post-surgical adhesion band formation

Arjmand

Hashemzehi

Soleimani

et al. 2021

Journal of Traditional and Complementary Medicine

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Background Abdominal adhesions are common and often develop after abdominal surgery. There are currently no useful targeted pharmacotherapies for adhesive disease. Saffron and its active constituents, Crocin and Crocetin, are wildly used in traditional medicine for alleviating the severity of inflammatory or malignant disease. Purpose The aim of this study was to investigate the therapeutic potential of the pharmacological active component of saffron in attenuating the formation of post-operative adhesion bands using different administration methods in a murine model. Material method saffron extract (100 mg/kg), Crocin (100 mg/kg), and Crocetin (100 mg/kg) were administered intraperitoneally and by gavage in various groups of male Wistar rat post-surgery. Also three groups were first treated intra-peritoneally by saffron extract, Crocin, and Crocetin (100 mg/kg) for 10 days and then had surgery. At the end of the experiments, animals sacrificed for biological assessment. Result A hydro-alcoholic extract of saffron and crocin but not crocetin potently reduced the adhesion band frequency in treatment and pre-treatment groups in the mice given intra-peritoneal (i.p) injections. Following the saffron or crocin administration, histological evaluation and quantitative analysis represented less inflammatory cell infiltration and less collagen composition, compared to control group. Moreover, the oxidative stress was significantly reduced in treatment groups. Conclusion These findings suggest that a hydro-alcoholic extract of saffron or its active compound, crocin, is a potentially novel therapeutic strategy for the prevention of adhesions formation and might be used as beneficial anti-inflammatory or anti-fibrosis agents in clinical trials. Taxonomy Abdominal surgeries/post-surgical adhesions.

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Section: Discussionsupporting

confidence: 92%

Therapeutic potential of active components of saffron in post-surgical adhesion band formation

Arjmand

Hashemzehi

Soleimani

et al. 2021

Journal of Traditional and Complementary Medicine

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“…Specifically, we found that GDFMD could effectively reverse the abnormal expression of 20 genes in WD; among these the expression of 18 genes (Apoa2, Acaa1b, Acsl1, Acox1, Ppara, Fads2, Scd2, Slc27a2, Pck1, Hmgcs2, Cyp7a1, Cyp4a31, Cyp4a14, Slc27a5, Slc27a1, Scd1, Cyp8b1, and Fabp1) was low and that of 2 genes (Cyp4a32 and Cyp4a10) was high in the Model group. A large body of evidence suggests that PPAR signaling pathway is involved in different liver diseases (Panebianco et al, 2017;Zhang et al, 2020), especially liver fibrosis (Chen et al, 2015;Pawlak et al, 2015;Chhimwal et al, 2020), as was also confirmed in the present study. Our results show that GDFMD can alleviate liver damage in WD by reversing the changes in the PPAR signaling pathway (Figure 8).…”

Section: Discussionsupporting

confidence: 89%

Comprehensive RNA-Seq Analysis of Potential Therapeutic Targets of Gan–Dou–Fu–Mu Decoction for Treatment of Wilson Disease Using a Toxic Milk Mouse Model

et al. 2021

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Background: Gan–Dou–Fu–Mu decoction (GDFMD) improves liver fibrosis in experimental and clinical studies including those on toxic mouse model of Wilson disease (Model). However, the mechanisms underlying the effect of GDFMD have not been characterized. Herein, we deciphered the potential therapeutic targets of GDFMD using transcriptome analysis.Methods: We constructed a tx-j Wilson disease (WD) mouse model, and assessed the effect of GDFMD on the liver of model mice by hematoxylin and eosin, Masson, and immunohistochemical staining. Subsequently, we identified differentially expressed genes (DEGs) that were upregulated in the Model (Model vs. control) and those that were downregulated upon GDFMD treatment (compared to the Model) using RNA-sequencing (RNA-Seq). Biological functions and signaling pathways in which the DEGs were involved were determined by gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) pathway analyses. A protein–protein interaction (PPI) network was constructed using the STRING database, and the modules were identified using MCODE plugin with the Cytoscape software. Several genes identified in the RNA-Seq analysis were validated by real-time quantitative PCR.Results: Total of 2124 DEGs were screened through the Model vs. control and Model vs. GDFMD comparisons, and dozens of GO and KEGG pathway terms modulated by GDFMD were identified. Dozens of pathways involved in metabolism (including metabolic processes for organic acids, carboxylic acids, monocarboxylic acids, lipids, fatty acids, cellular lipids, steroids, alcohols, eicosanoids, long-chain fatty acids), immune and inflammatory response (such as complement and coagulation cascades, cytokine–cytokine receptor interaction, inflammatory mediator regulation of TRP channels, antigen processing and presentation, T-cell receptor signaling pathway), liver fibrosis (such as ECM-receptor interactions), and cell death (PI3K-Akt signaling pathway, apoptosis, TGF-beta signaling pathway, etc.) were identified as potential targets of GDFMD in the Model. Some hub genes and four modules were identified in the PPI network. The results of real-time quantitative PCR analysis were consistent with those of RNA-Seq analysis.Conclusions: We performed gene expression profiling of GDFMD-treated WD model mice using RNA-Seq analysis and found the genes, pathways, and processes effected by the treatment. Our study provides a theoretical basis to prevent liver fibrosis resulting from WD using GDFMD.

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“…It has also been confirmed that PPAR-γ plays a strong role in inhibiting liver fibrosis by cross-talk with inflammatory-related factors, such as NF-κB and AP-1, inhibiting T cell activation and macrophage proliferation and secretion. 4 , 28 , 38 , 39 …”

Section: Mechanisms Underlying Hepatic Fibrosis and Ppar-γmentioning

confidence: 99%

“… 78 Crocin treatment significantly reduces the serum liver enzyme level and improves liver CYP2E1 mRNA levels and the pathologic changes of liver tissue. 38 The alcohol extract of Rhus verniciflua fruit can prevent liver fibrosis induced by carbon tetrachloride in mice by inhibiting inflammatory factors [83]. Lycopene inhibits HSC activation, and regulates cell lipid storage and signal transduction.…”

Section: Ppar-γ Targets Anti-fibrosis Drugsmentioning

confidence: 99%

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The Agonists of Peroxisome Proliferator-Activated Receptor-γ for Liver Fibrosis

Li¹,

Guo²,

Wu³

2021

DDDT

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Liver fibrosis is a common link in the transformation of acute and chronic liver diseases to cirrhosis. It is of great clinical significance to study the factors associated with the induction of liver fibrosis and elucidate the method of reversal. Peroxisome proliferator-activated receptors (PPARs) are a class of nuclear transcription factors that can be activated by peroxisome proliferators. PPARs play an important role in fibrosis of various organs, especially the liver, by regulating downstream targeted pathways, such as TGF-β, MAPKs, and NF-κB p65. In recent years, the development and screening of PPAR-γ ligands have become a focus of research. The PPAR-γ ligands include synthetic hypolipidemic and antidiabetic drugs. In addition, microRNAs, lncRNAs, circRNAs and nano new drugs have attracted research interest. In this paper, the research progress of PPAR-γ in the pathogenesis and treatment of liver fibrosis was discussed based on the relevant literature in recent years.

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Crocin attenuates CCl₄-induced liver fibrosis via PPAR-γ mediated modulation of inflammation and fibrogenesis in rats

Cited by 37 publications

References 36 publications

Therapeutic potential of active components of saffron in post-surgical adhesion band formation

Therapeutic potential of active components of saffron in post-surgical adhesion band formation

Comprehensive RNA-Seq Analysis of Potential Therapeutic Targets of Gan–Dou–Fu–Mu Decoction for Treatment of Wilson Disease Using a Toxic Milk Mouse Model

The Agonists of Peroxisome Proliferator-Activated Receptor-γ for Liver Fibrosis

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Crocin attenuates CCl4-induced liver fibrosis via PPAR-γ mediated modulation of inflammation and fibrogenesis in rats

Cited by 37 publications

References 36 publications

Therapeutic potential of active components of saffron in post-surgical adhesion band formation

Therapeutic potential of active components of saffron in post-surgical adhesion band formation

Comprehensive RNA-Seq Analysis of Potential Therapeutic Targets of Gan–Dou–Fu–Mu Decoction for Treatment of Wilson Disease Using a Toxic Milk Mouse Model

The Agonists of Peroxisome Proliferator-Activated Receptor-γ for Liver Fibrosis

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Crocin attenuates CCl₄-induced liver fibrosis via PPAR-γ mediated modulation of inflammation and fibrogenesis in rats