scholarly journals ATTENUATION OF CARBON TETRACHLORIDE AND ETHANOL-INDUCED HEPATIC FIBROSIS IN RATS BY CALLIGONUM COMOSUM SHOOT EXTRACT

2017 ◽  
Vol 10 (3) ◽  
pp. 83
Author(s):  
Amria Mamdouh Mousa ◽  
Sherien Kamal Hassan ◽  
Nermin Mohammed El-sammad
Keyword(s):  
Body Weight ◽  
Carbon Tetrachloride ◽  
Liver Fibrosis ◽  
Matrix Metalloproteinase ◽  
Hepatic Fibrosis ◽  
Methanolic Extract ◽  
Elevated Serum ◽  
Matrix Metalloproteinase 2 ◽  
Ccl4 Administration ◽  
Liver And Kidney

ABSTRACTObjective: This study was designed to evaluate the hepatoprotective and antioxidant effects of methanolic extract of Calligonum comosum (C. comosum)shoots on the hepatic fibrosis induced by carbon tetrachloride and ethanol (CCl4/ethanol) in rats.Methods: A liver fibrosis was induced in Sprague Dawley rats by oral administration of CCl4 (1 ml/kg body weight, twice weekly for 10 weeks) alongwith ethanol (10% in drinking water 1 week before CCl4 administration and throughout the experiment). Rats were pretreated with C. comosumextract (daily, orally at a dose of 50 mg/kg body weight 1 week before CCl4 administration). At the end of the experiment, serum, and liver sampleswere subjected to biochemical investigations. In addition, liver and kidney tissues were evaluated for histopathological changes.Results: C. comosum extract pretreatment significantly reduced CCl4 - induced elevation in serum levels of aspartate aminotransaminase, alanineaminotransaminase, alkaline phosphatase, total bilirubin, urea, creatinine, and significantly elevated serum contents of total protein and albumin, aswell as an improvement in hepatic protein content, albumin/globulin ratio, body weight and relative liver and kidney weights. C. comosum extract alsosignificantly increased the hepatic levels of glucose-6-phosphatase, glutathione peroxidase, glutathione-S-transferase, catalase, superoxide dismutase,and glutathione with significant decrease in the contents of malondialdehyde and protein carbonyl. In addition, downregulation in expression ofthe fibrotic marker matrix metalloproteinase-2 was observed. C. comosum extract also ameliorated histopathological changes of CCl4/ethanol groupwhich further evidenced the biochemical findings.Conclusion: Our results confirmed that the methanolic extract of C. comosum shoots effectively protect against CCl4/ethanol-induced liver fibrosis,through its antioxidant property.Keywords: Calligonum comosum, Hepatic fibrosis, Carbon tetrachloride, Hepatoprotective effect, Antioxidants, Matrix metalloproteinase-2.

scholarly journals Evaluation of hepatoprotective effect of Waltheria indica against various NSAIDs-induced hepatic damage in rats

2017 ◽  
Vol 9 (1) ◽  
pp. 157 ◽  
Author(s):  
Amol Chandekar ◽  
Neeraj Upamanyu ◽  
Amber Vyas ◽  
Atul Tripathi ◽  
Surendra Agrawal ◽  
...  
Keyword(s):  
Body Weight ◽  
Carbon Tetrachloride ◽  
Traditional Medicine ◽  
Hepatic Fibrosis ◽  
Methanolic Extract ◽  
Hepatoprotective Activity ◽  
Histopathological Analysis ◽  
Standard Drug ◽  
Blood Samples ◽  
Liver Disorders

<p>The objective of the present study was to evaluate methanolic extract of leaves of Waltheria indica linn. for hepatoprotective potency of the potent solvent extract. The hepatotoxicity was induced by diclofenac, carbon tetrachloride (CCl 4 ) and acetaminophen. In CCl 4 induced hepatotoxicity study, animals were divided into five groups (n=6). Methanolic extract of Waltheria indica (WIM) groups were injected in doses of 400 mg/kg and 600mg/kg body weight along with CCl 4 and Silymarin 100mg/kg was taken as standard drug. Similarly procedure was followed in diclofenac and acetaminophen induced hepatotoxicity. Blood samples and liver were collected and liver hisopathological studies were carried out. These histopathological analysis suggested that WIM extract have the ability to reduce the degree of hepatic fibrosis induced by various factors. And concluded that WIM extract has significant hepatoprotective activity thus this study scientifically support the theory to use of this plant in traditional medicine for the treatment of liver disorders.</p>

scholarly journals Comparative Protective Effects of Spirulina and Spirulina Supplemented with Thiamineagainst Sub-acute Carbon Tetrachloride Toxicity in Rats

2019 ◽  
Vol 12 (2) ◽  
pp. 511-526
Author(s):  
Badr E. El-Bialy ◽  
Neveen G. El-Boraey ◽  
Ragaa A. Hamouda ◽  
Mohamed M. Abdel-Daim
Keyword(s):  
Body Weight ◽  
Carbon Tetrachloride ◽  
Spirulina Platensis ◽  
Body Weight Gain ◽  
Ros Generation ◽  
Protective Effects ◽  
Blood Indices ◽  
Indirect Bilirubin ◽  
Liver And Kidney ◽  
Haemoglobin Content

Carbon tetrachloride (CCl4) is used extensively as an industrial solvent and considered the best-characterized experimental animal model of xenobiotic-induced hepatic toxicity via reactive oxygen species (ROS) generation. This study was designed to evaluate the protective effects of Spirulina platensis (SP) versus Spirulina platensis supplemented with thiamine (SPt) against subacute CCl4 toxicity in rats. Rats were divided into six equal groups; Control vehicle (0.5 ml/rat 1:1 olive oil in water), SP (800 mg/kg b.wt.), SPt (800 mg/kg b.wt.), CCl4 (1ml/kg b.wt.), SP + CCl4 and SPt + CCl4. All treatments were orally and daily for a month except CCl4 was given three times weekly. CCl4 caused significant reduction in body weight gain, haemoglobin content and haematocrit percentage accompanied by leukocytosis, granulocytosis, monocytosis and lymphocytopenia. Moreover, there were significant increase in the levels of serum ALT, AST; total, direct and indirect bilirubin; urea and creatinine of CCL4- intoxicated rats. CCL4- induced significant increase of malondialdehyde levels with significant reduction of catalase activity in liver and kidney. In addition, hepatic and renal various histopathological alterations were recorded. SP and SPt ameliorated almost these changes while they couldn’t reverse the reduction of body weight gains and red blood indices. The more potent effects on measured parameters were elucidated by SPt. In conclusion SP and SPt could be used as natural antioxidant supplements to counteract the CCl4 adverse effects.

Matrix metalloproteinase-2 activation in human hepatic fibrosis regulation by cell-matrix interactions

Hepatology ◽  
1999 ◽  
Vol 30 (4) ◽  
pp. 944-950 ◽  
Author(s):  
Anne-Marie Préaux ◽  
Ariane Mallat ◽  
Jeanne Tran Van Nhieu ◽  
Marie-Pia d'Ortho ◽  
Rosalind M. Hembry ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Hepatic Fibrosis ◽  
Matrix Metalloproteinase 2 ◽  
Cell Matrix ◽  
Matrix Interactions ◽  
Cell Matrix Interactions

scholarly journals Inhibition of Mastermind-like 1 alleviates liver fibrosis induced by carbon tetrachloride in rats

2018 ◽  
Vol 243 (14) ◽  
pp. 1099-1108
Author(s):  
Shaoping Zheng ◽  
Yixiong Chen ◽  
Shaojiang Zheng ◽  
Zhihui He ◽  
Zhihong Weng
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Fibrosis ◽  
Hepatic Fibrosis ◽  
Hepatic Stellate Cells ◽  
Stellate Cells ◽  
Underlying Mechanism ◽  
Signal Pathways ◽  
Fibrotic Liver ◽  
Hepatic Fibrogenesis ◽  
Signal Transductions

Mastermind-like 1 (MAML1) functions in critical transcriptional coactivation in Notch and Wnt/β-catenin signal pathways, which participate in hepatic fibrosis. This study is aimed to reveal the potential role of MAML1 in liver fibrosis and identify its underlying mechanism. In present research, the enhanced expression of MAML1 was found in the fibrotic liver tissues in carbon tetrachloride (CCl4)-induced hepatic fibrosis in rats, and MAML1 expression increased gradually during the activation of hepatic stellate cells (HSCs) isolated from the normal rat. Further studies showed that blocking MAML1 expression efficiently decreased the expression of α-SMA and collagen I (Col1a1) in HSCs. Interestingly, MAML1 may modulate HSCs activation via interrupting both Notch and Wnt/β-catenin signal transductions, and the inhibition of MAML1 by a recombinant adeno-associated virus type 1 vector carrying shRNA targeting MAML1 alleviated CCl4-induced hepatic fibrosis in rats. These findings suggest that the selective regulation of MAML1 expression may be a feasible therapeutic approach to reverse liver fibrosis. Impact statement Liver fibrosis is a common wound-healing response to all kinds of liver injuries. Hepatic stellate cells (HSCs) activation is the key event during liver fibrogenesis. Thus, the elucidation of mechanisms for regulating HSCs activation is helpful for identifying novel anti-fibrotic targets and strategies. MAML1, an important component of Notch signal, functions in critical transcriptional coactivation in the Notch and Wnt/β-catenin signal pathways. In the present study, we investigated the potential function of MAML1 during hepatic fibrogenesis in rats. Our results demonstrated that MAML1 participates in liver fibrosis through modulating HSCs activation via interrupting both the Notch and Wnt/β-catenin signal transductions. Additionally, the inhibition of MAML1 markedly attenuated CCl4-induced hepatic fibrogenesis in rats. Our results shed a light for the exploitation of a new therapeutic strategy for hepatic fibrosis via targeting MAML1.

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