Immunological tolerance to pig-serum partially inhibits the formation of septal fibrosis of the liver in Capillaria hepatica-infected rats

Andrade, Rodrigo Guimarães; Gotardo, Bruna Magalhães; Assis, Bárbara C.A.; Mengel, José; Andrade, Zilton A.

doi:10.1590/s0074-02762004000700007

Cited by 4 publications

(3 citation statements)

References 19 publications

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“…The procedure of dividing the animals into groups and for the generation of the PS-induced model of liver fibrosis was based on the method described previously, with certain modifications (14,15). Animals were weighed once per week, and 24 h after the final injection of PS all animals were sacrificed under anesthesia with ether.…”

Section: Methodsmentioning

confidence: 99%

Anti-fibrotic effects of Acremoniumterricola milleretal mycelium on immunological hepatic fibrosis in rats

et al. 2014

Molecular Medicine Reports

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Abstract. Acremoniumterricola milleretal mycelium (AMM) exerts numerous protective effects on organs, and has been used in Chinese herb prescriptions to treat refractory diseases. The aim of this study was to investigate the effects of AMM on immunological hepatic fibrosis induced by porcine serum (PS) in rats. Male Sprague Dawley rats were administered 0.5 ml sterile PS by intraperitoneal injections twice a week for 18 weeks. AMM (175, 350 or 700 mg/kg) and colchicine (0.1 mg/kg) were administered intragastrically each day until the rats were sacrificed. PS administration resulted in marked hepatic fibrosis, as assessed by increased oxidative stress and hepatic collagen content, as well as α-smooth muscle actin (α-SMA) expression. AMM significantly reduced liver damage and fibrosis. In addition, AMM decreased the elevation in hydroxyproline, hyaluronic acid, laminin and procollagen type III; increased the activity of superoxide dismutase and glutathione peroxidase; decreased α-SMA expression; and eliminated hepatic collagen deposits. Furthermore, AMM inhibited Smad2/3 phosphorylation and Smad7 expression. These results indicate that AMM is able to reduce oxidative stress, inhibit collagen synthesis and block the transforming growth factor-β/Smad signaling pathway in a dose-dependent manner.

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Section: Methodsmentioning

confidence: 99%

Anti-fibrotic effects of Acremoniumterricola milleretal mycelium on immunological hepatic fibrosis in rats

et al. 2014

Molecular Medicine Reports

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“…As an antigen substance, xenogeneic serum induces an immunoresponse in the liver, leading to the formation of immune complexes. If the excessive immune complexes are not removed in a timely manner, they are deposited in the liver and the hepatic vascular wall, causing cell infiltration, release of inflammatory mediators, cell degeneration of parenchymal liver cells, fibrous hyperplasia and hepatic fibrosis (27,29,30). The present study developed an in vivo model of hepatic fibrosis in rats using porcine serum.…”

Section: β-Hydroxysteroid Dehydrogenase-1 Is Associated With the Acmentioning

confidence: 98%

11β‑hydroxysteroid dehydrogenase‑1 is associated with the activation of hepatic stellate cells in the development of hepatic fibrosis

Xiao

Rong

et al. 2020

Mol Med Rep

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Hepatic fibrosis (HF) is a common complication of numerous chronic liver diseases, but predominantly results from persistent liver inflammation or injury. If left untreated, HF can progress and develop into liver cirrhosis and even hepatocellular carcinoma. However, the underlying molecular mechanisms of HF remain unknown. The present study aimed to investigate the role of 11β-hydroxysteroid dehydrogenase-1 (11β-HSD1) during the development of hepatic fibrosis. An experimental rat model of liver fibrosis was induced using porcine serum. 11β-HSD1 gene expression levels and enzyme activity during hepatic fibrogenesis were assessed. 11β-HSd1 gene knockdown using small interfering RNA and overexpression were performed in LX2-human hepatic stellate cells (HSCs). HSCs were stimulated with transforming growth factor-β1 (TGF-β1). Cell cycle distribution, proliferation, collagen secretion and 11β-HSD1 gene activity in HSCs were compared before and after stimulation. As hepatic fibrosis progressed, 11β-HSD1 gene expression and activity increased, indicating a positive correlation with typical markers of liver fibrosis. 11β-HSD1 inhibition markedly reduced the degree of fibrosis. The cell proliferation was increased, the number of cells in the G 0 /G 1 phase decreased and the number of cells in the S and G 2 /M phases increased in the pSuper transfected group compared with the N group. In addition, the overexpression of 11β-HSD1 enhanced the TGF-β1-induced activation of LX2-HSCs and enzyme activity of connective tissue growth factor. 11β-HSD1 knockdown suppressed cell proliferation by blocking the G 0 /G 1 phase of the cell cycle, which was associated with HSC stimulation and inhibition of 11β-HSd1 enzyme activity. In conclusion, increased 11β-HSD1 expression in the liver may be partially responsible for hepatic fibrogenesis, which is potentially associated with HSC activation and proliferation.

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“…The experimental model for hepatic septal fibrosis, which invariably develops in rats following infection with the nematode Capillaria hepatica, has already been applied to the study of several aspects of the pathogenesis of hepatic fibrosis [1][2][3][4][5][6] since its first description in 1993 7 . One advantage of this experimental method lies on its regularity of development, since hepatic fibrosis starts around 16-20 days following infection, establishing portal to portal connections and soon involving the entire liver.…”

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confidence: 99%

Capillaria hepatica-induced septal fibrosis in rats: a contribution to the study of liver fibrogenesis

Barbosa

Andrade

2010

Rev. Soc. Bras. Med. Trop.

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INTRODUCTION: Septal fibrosis of the liver regularly develops in rats infected with the nematode Capillaria hepatica. Curative treatment of the infection prevents the development of septal fibrosis when intervention occurs up to postinfection day (PID) 15, but not later. The present investigation aimed to demonstrate which parasitic factors are present when the process of septal fibrosis can no longer be prevented by curative treatment. METHODS: Wistar rats were infected with 600 embryonated eggs of C. hepatica administered by gavage and treated with ivermectin and mebendazole in separate groups at PIDs 10, 12, 15, 17 or 20. Rats from each group and their nontreated controls, were killed and examined 40 days after the end of treatment. RESULTS: Findings by PID 15 were compatible with the stage of complete maturation of infection, when worms and eggs were fully developed and a complex host-parasite multifocal necroinflammatory reaction showed greater intensity, but with no signs of septal fibrosis, which appeared from PID 17 onward. CONCLUSIONS: Since the worms spontaneously died by PID 15, not only septal fibrosis production, but also its maintenance and further development appeared dependent on the presence of eggs, which were the only parasitic factor remaining thereafter.

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Immunological tolerance to pig-serum partially inhibits the formation of septal fibrosis of the liver in Capillaria hepatica-infected rats

Cited by 4 publications

References 19 publications

Anti-fibrotic effects of Acremoniumterricola milleretal mycelium on immunological hepatic fibrosis in rats

Anti-fibrotic effects of Acremoniumterricola milleretal mycelium on immunological hepatic fibrosis in rats

11β‑hydroxysteroid dehydrogenase‑1 is associated with the activation of hepatic stellate cells in the development of hepatic fibrosis

Capillaria hepatica-induced septal fibrosis in rats: a contribution to the study of liver fibrogenesis

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