&lt;b&gt;Modelos experimentais para indução de cirrose hepática em animais: Revisão de literatura&lt;/b&gt;&lt;br&gt;doi: 10.5007/2175-7925.2010v23n2p183

Passos, Cristiane Carlin; Ferreira, Amanda Olivotti; Blazquez, Francisco Javier Hernandez; Guerra, Ricardo Romão

doi:10.5007/2175-7925.2010v23n2p183

Cited by 5 publications

(4 citation statements)

References 36 publications

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“…Chronic liver disease and liver fibrosis have always been the focus of contemporary medical research, and people have tried to establish a model of liver fibrosis to adapt to contemporary research needs in recent years ( Sepanlou et al, 2020 ). As a potent hepatotoxin, TAA-induced liver fibrosis is a well-recognised model for the development of liver damage, regenerative nodules and fibrosis, similar to human liver fibrosis ( Passos et al, 2010 ; Nascimento et al, 2018 ). Numerous experiments have shown that long-term administration of TAA leads to proliferative liver nodules, liver fibrosis, hepatocellular adenomas and hepatocellular carcinoma ( Li et al, 2002 ; Yeh et al, 2004 ; Constantinou et al, 2007 ; Jantararussamee et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Dihydromyricetin Reverses Thioacetamide-Induced Liver Fibrosis Through Inhibiting NF-κB-Mediated Inflammation and TGF-β1-Regulated of PI3K/Akt Signaling Pathway

et al. 2021

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As a natural active substance, dihydromyricetin (DHM) has been proven to have good hepatoprotective activity. However, the therapeutic effect of DHM on liver fibrosis, which has become a liver disease threatening the health of people around the world, has not been studied to date. The purpose of this study was to investigate the effect of DHM as a new nutritional supplement on thioacetamide (TAA)-induced liver fibrosis. The liver fibrosis model was established by intraperitoneal injection of TAA (200 mg/kg, every 3 days) for 8 weeks, and oral administration of DHM (20 mg/kg and 40 mg/kg, daily) after 4 weeks of TAA-induced liver fibrosis. The results showed that DHM treatment significantly inhibited the activities of alanine aminotransferase (ALT) (37.81 ± 7.62 U/L) and aspartate aminotransferase (AST) (55.18 ± 10.94 U/L) in serum of liver fibrosis mice, and increased the levels of superoxide dismutase (SOD) and glutathione (GSH) while reversed the level of malondialdehyde (MDA). In addition, histopathological examination illustrated that TAA induced the inflammatory infiltration, apoptosis and fibroatherosclerotic deposition in liver, which was further confirmed by western-blot and immunofluorescence staining. Moreover, DHM inhibited hepatocyte apoptosis by regulating the phosphorylation level of phosphatidylinositol 3-kinase (PI3K), protein kinase-B (AKT) and its downstream apoptotic protein family. Interestingly, immunofluorescence staining showed that DHM treatment significantly inhibited alpha smooth muscle actin (α-SMA), which was a marker of hepatic stellate cell activation, and regulated the expression of transforming growth factor (TGF-β1). Importantly, supplementation with DHM significantly inhibited the release of nuclear factor kappa-B (NF-κB) signaling pathway and pro-inflammatory factors in liver tissue induced by TAA, and improved liver fiber diseases, such as tumor necrosis factor alpha (TNF-α) and recombinant rat IL-1β (IL-1β). In conclusion, the evidence of this study revealed that DHM is a potential hepatoprotective and health factor, and which also provides the possibility for the treatment of liver fibrosis.

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Section: Introductionmentioning

confidence: 99%

Dihydromyricetin Reverses Thioacetamide-Induced Liver Fibrosis Through Inhibiting NF-κB-Mediated Inflammation and TGF-β1-Regulated of PI3K/Akt Signaling Pathway

et al. 2021

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“…Chemical procedures are developed through the administration of hepatotoxic substances. Among several experimental models of cirrhosis induction, TAA, a drug originally used as a fungicide to protect oranges against deterioration and later recognized as a potent hepatotoxin, has been the most promising because it produces macroscopic and histological morphological patterns similar to cirrhosis in human beings (Passos et al 2010).…”

Section: Macroscopic and Histological Assessmentmentioning

confidence: 99%

Hepatoprotective and antineoplastic potencial of red propolis produced by the bees Apis mellifera in the semiarid of Rio Grande do Norte, Brazil

et al. 2019

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The objective of this study was to evaluate the hepatoprotective effect of the honey bee Apis mellifera ethanolic extract of the red propolis, obtained in four municipalities of the Rio Grande do Norte semi-arid region, through an in vitro evaluation of the antineoplastic potential in human hepatic carcinoma (HepG2) and normal cell lines (L929), and from the comet assay in hepatic cell lines (ZF-L hepatocytes) to evaluate the genoprotective potential of the extract. The hepatoprotective effect was also evaluated in vivo by the induction of chronic experimental hepatic lesions in rodents (Rattus norvegicus Berkenhout, 1769), Wistar line, by intraperitoneal administration of thioacetamide (TAA) at the dose of 0.2g/kg. The animals were distributed in the following experimental groups: G1 (control), G2 (treated with 500mg/kg ethanolic extract of propolis), G3 (treated with 500mg/kg of ethanolic extract and TAA) and G4 (treated with TAA). All rats were submitted to serum biochemical, macroscopic, histological and stereological biochemical exams of the liver. It was verified the genoprotective effect of red propolis since the mean damages promoted to DNA in cells tested with the extract were significantly lower than the mean of the positive control damage (hydrogen peroxide). The red propolis extract did not present cytotoxic activity to the tumor cells of human liver cancer, as well as to normal ones. The absence of cytotoxicity in normal cells may indicate safety in the use of the propolis extract. The results of the serum biochemical evaluation showed that the serum levels of the aminotransferase enzymes (AST) did not differ significantly between G1, G2 and G3 when compared to each other. G4 showed significant increase in levels compared to the other groups, indicating that the administration of the extract did not cause liver toxicity, as well as exerted hepatoprotective effect against the hepatic damage induced by TAA. The G3 and G4 animals developed cirrhosis, but in G3 the livers were characterized by the presence of small regenerative nodules and level with the surface of the organ, whereas in G4 the livers showed large regenerative nodules. The livers of the G1 and G2 animals presented normal histological appearance, whereas the livers of the G3 animals showed regenerative nodules surrounded by thin septa of connective tissue, and in G4 the regenerative nodules were surrounded by thick septa fibrous connective tissue. The analysis of the hepatic tissues by means of stereology showed that there was no statistical difference between the percentage of hepatocytes, sinusoids, and collagens in G1 and G2. In G3 the percentage of hepatocytes, sinusoids, and collagen did not differ significantly from the other groups. It was concluded that the ethanolic extract of the red propolis exerted a hepatoprotective effect, because it promoted in vitro reduction of the damage to the DNA of liver cells, antineoplastic activity in human hepatocellular carcinoma cell line (HepG2) and did not exert cytotoxic effect in normal cells or was able to reduce liver enzyme activity and the severity of cirrhosis induced by TAA in vivo.

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“…A repetição de um dano tóxico ao fígado é uma estratégia clássica para indução de fibrose e cirrose hepática em animais experimentais (Starkel e Leclercq, 2011). As principais drogas utilizadas para tal fim incluem D-galactosamina, tetracloreto de carbono (CCl 4 ), tioacetamida (TAA) e dimetilnitrosamina (DMN), entre outras, que são administradas por via oral ou por injeção intraperitoneal em diferentes concentrações e em aplicações que podem ser únicas ou semanais com duração de meses (Passos et al, 2011;Tunon et al, 2009).…”

Section: -Modelos Animais De Fibrose E Cirrose Hepáticaunclassified

Diferenciação de células-tronco em hepatócitos e desenvolvimento de modelo pré-clínico de fibrose hepática para ensaios de terapia celular

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<b>Modelos experimentais para indução de cirrose hepática em animais: Revisão de literatura</b><br>doi: 10.5007/2175-7925.2010v23n2p183

Cited by 5 publications

References 36 publications

Dihydromyricetin Reverses Thioacetamide-Induced Liver Fibrosis Through Inhibiting NF-κB-Mediated Inflammation and TGF-β1-Regulated of PI3K/Akt Signaling Pathway

Dihydromyricetin Reverses Thioacetamide-Induced Liver Fibrosis Through Inhibiting NF-κB-Mediated Inflammation and TGF-β1-Regulated of PI3K/Akt Signaling Pathway

Hepatoprotective and antineoplastic potencial of red propolis produced by the bees Apis mellifera in the semiarid of Rio Grande do Norte, Brazil

Diferenciação de células-tronco em hepatócitos e desenvolvimento de modelo pré-clínico de fibrose hepática para ensaios de terapia celular

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