Liver fibrosis in mice induced by carbon tetrachloride and its reversion by luteolin

Domitrović, Robert; Jakovac, Hrvoje; Tomac, Jelena; Šain, Ivana

doi:10.1016/j.taap.2009.09.001

Cited by 106 publications

(88 citation statements)

References 62 publications

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“…These findings were in line with the previous reports of Domitrović et al [41] who stated that liver fibrosis was characterised by activated HSC with accelerated proliferation and enhanced production of ECM components. Hepatic stellate cell activation involves the trans-differentiation from a quiescent state into myofibroblast-like cells with the appearance of α-SMA and loss of cellular vitamin A storage.…”

Section: Discussionsupporting

confidence: 93%

Ameliorative Effect of Hesperidin on Carbon Tetrachloride Induced Liver Fibrosis in Rats

Abdel-sttar

Khalaf

Abo-Youssef

et al. 2017

Int J Pharm Pharm Sci

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Objective: Exposure to carbon tetrachloride leads to serious liver injury and fibrosis. This study was aimed to evaluate the hepatoprotective effects of hesperidin against carbon tetrachloride (CCl4)-induced liver fibrosis in rats compared with the reference drug silymarin.Methods: Wistar albino rats were divided into five groups, each of eight rats. Animals were allocated into a control group, corn oil group and fibrosis control group. The remaining two groups received in addition to CCl4, silymarin (100 mg/kg/d) as a reference treatment and hesperidin (200 mg/kg/d). At the end of experimental period, the biomarkers of specific fibrosis [hepatic transforming growth factor β1 (TGF-β1) and hydroxyproline (HYP)], liver function [serum alanine transaminase (ALT), aspartate transaminase (AST), albumin and total bilirubin], oxidative stress [hepatic malondialdehyde (MDA), glutathione (GSH) and catalase (CAT)], inflammatory [hepatic myeloperoxidase (MPO), serum tumor necrosis factor alpha (TNF-α)], relative liver weight, lipid profile [total cholesterol, serum triglycerides, high-density lipoprotein cholesterol (HDLCh) and low density lipoprotein cholesterol (LDL-Ch)] were evaluated, supported by liver histopathological study and immunohistochemistry of alpha-smooth muscle actin (α-SMA) in liver sections.Results: Hesperidin significantly decreased hepatic transforming growth factor β1, hydroxyproline, the serum liver function markers of ALT, AST and total bilirubin, the hepatic content of MDA and MPO activity, the serum pro-inflammatory cytokine TNF-α, relative liver weight, and the serum lipid profile markers cholesterol, triglycerides and LDL. On the other hand, Hesperidin significantly increased albumin, the hepatic content of GSH and CAT, and serum lipid profile of LDL. In addition, liver sections obtained from these groups showed marked histopathological and immunohistochemistry of α-SMA improvement. Conclusion:Hesperidin may be promising protective agent against liver fibrosis through improvement of liver function, modulation of the fibrous scar formation, anti-inflammatory and antioxidant potentials.

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Section: Discussionsupporting

confidence: 93%

Ameliorative Effect of Hesperidin on Carbon Tetrachloride Induced Liver Fibrosis in Rats

Abdel-sttar

Khalaf

Abo-Youssef

et al. 2017

Int J Pharm Pharm Sci

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“…In our model, the level of serum ALT increased sharply in the context of hepatitis and acute liver injury. The results of AST and ALT levels in the control group were consistent with other reports (Domitrovic et al, 2009). In group I, we observed insignificant changes in serum ALT and AST before and after CCl4 treatment, suggesting that injured liver cells were likely to be restored because of low CCl4 concentrations (Mederacke, 2013).…”

Section: Discussionsupporting

confidence: 91%

“…Although no model that specifically represent the etiologies of human liver cirrhosis have been developed, several animal models of human liver diseases are currently used, including models induced by hepatotoxins, carbon tetrachloride (CCl 4 ) (Domitrovic et al, 2009;Ming-Ling Chang, 2005), 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) (Ming-Ling Chang, 2005), silica, allyl alcohol (AA), alpha-naphthyl-isothiocyanate (ANIT), and bile duct ligation. These models have provided support for our understanding of the mechanisms of hepatic fibrosis and have enabled us to evaluate the safety and effectiveness of novel potential therapies for liver fibrosis and cirrhosis (Ming-Ling Chang, 2005;Starkel and Leclercq, 2011;Yan Liu, 2013).…”

Section: Introductionmentioning

confidence: 99%

Establishment of a standardized mouse model of hepatic fibrosis for biomedical research

Truong¹,

Nguyen²,

Nguyen³

et al. 2014

Biomed Res Ther

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Abstract-Liver injury causes nodule and scar tissue formation and diffuse fibrosis, which are characteristic of liver cirrhosis. Since there are currently no efficacious therapies to prevent fibrosis, the development of animal models of liver fibrosis is necessary to facilitate further in vivo studies of this pathology. In this study, a mouse model of liver fibrosis was generated using Swiss mice and carbon tetrachloride (CCl 4 ) treatment. Induction of liver fibrosis was analyzed using 0.8, 1.0, or 1.2 mL/kg CCl 4 to determine the effective dose. In this study, we aimed to develop a standardized hepatic fibrosis mouse model by using CCl 4 induction to facilitate further studies in this field. In Swiss mice, we evaluated the dose of CCl 4 and the criteria of fibrosis, such as serum markers, fibrosis marker genes, and histopathology. Mice were administered CCl 4 three times per week for 8 consecutive weeks. Body weights, survival rates, levels of serum markers (aspartate aminotransferase/alanine aminotransferase [AST/ALT]) and fibrosis markers (fibronectin, procollagen, nt5e, transforming growth factor-beta [TGF-β], and integrin), and histopathology (using hematoxylin and eosin [H&E] staining) were analyzed to determine the optimal dose of CCl 4 for induction of liver fibrosis. Results showed that 1.0 mL/kg CCl 4 was the most efficient dose for the establishment of a liver fibrosis mouse model. In a standardized liver fibrosis model, mice were treated with 1.0 mL/kg CCl 4 three times per week for 11 consecutive weeks, and levels of serum markers (AST, ALT, bilirubin, and albumin), expression of fibrosis marker genes (using quantitative reverse transcription polymerase chain reaction [RT-PCR]), histopathology (using Hematoxylin and eosin staining), and connective tissue formation (using Massive trichrome staining) were analyzed. The outcomes showed that serum markers and the levels of fibrosis marker genes were significantly increased in the standardized liver fibrosis model. Additionally, we observed sharp increases in fibronectin and procollagen expression (1222.40 ± 4.20 and 241.35 ± 1.18, respectively), and the development of cirrhosis (fibrosis stage 3-5/6) in liver tissues of the standardized mouse model of hepatic fibrosis.

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“…Moreover, Masson's trichrome stain of liver sections showed congestion and thickening of the portal tract with dense fibrous tissue. Similar observations of the liver tissues in CCl 4 intoxicated rats were reported previously (Domitrovic et al, 2009;Althnaian et al, 2013).…”

Section: Discussionsupporting

confidence: 90%

Synergistic Effects of Jerusalem Artichoke in Combination with Pegylated Interferon Alfa-2a and Ribavirin Against Hepatic Fibrosis in Rats

Abdel-Hamid

Wahid²,

Nazmy³

et al. 2016

Asian Pacific Journal of Cancer Prevention

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Liver fibrosis in mice induced by carbon tetrachloride and its reversion by luteolin

Cited by 106 publications

References 62 publications

Ameliorative Effect of Hesperidin on Carbon Tetrachloride Induced Liver Fibrosis in Rats

Ameliorative Effect of Hesperidin on Carbon Tetrachloride Induced Liver Fibrosis in Rats

Establishment of a standardized mouse model of hepatic fibrosis for biomedical research

Synergistic Effects of Jerusalem Artichoke in Combination with Pegylated Interferon Alfa-2a and Ribavirin Against Hepatic Fibrosis in Rats

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