Functional state of the hematopoietic system in different stages of CCl4-induced liver fibrosis in mice

Zubakhin, A. A.; Kutina, S. N.; Mayanskii, D. N.

doi:10.1007/bf00790046

Cited by 3 publications

(4 citation statements)

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“…Mice and rats were killed when known as inducing fibrotic stage by CCl 4 administration. [17][18][19] H. pylori infection for 4 months caused functional and morphological degenerative changes in hepatocytes, such as the depletion of glycogen particles, hydropic degeneration, binucleation and accumulation of numerous small fat droplets in our present research (Figures 7 and 8). These histological findings regarding hepatocytes suggest that H. pylori causes a disarrangement of hepatic architecture with some showing slight focal necrosis and inflammatory changes in spite of there being no severe hepatitis present in the liver samples used in this study (Figure 7).…”

Section: Discussionsupporting

confidence: 60%

“…CCl 4 was administered for 15 weeks as a previously described regimen to induce liver fibrosis. 18,19 In these animal models, CCl 4 treatment was conducted after the first week, when inoculation of the mice with H. pylori was initiated. Mice were infected with H. pylori strain SS1, 0.2 ml of inoculum per mouse, killed at the end of the sixteenth week and then their organs were collected as described above.…”

Section: Experimental Design-2mentioning

confidence: 99%

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Helicobacter pylori promotes hepatic fibrosis in the animal model

Goo

Lee

et al. 2009

Laboratory Investigation

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Helicobacter pylori infection has been reported to be very common in patients with chronic liver diseases, including cirrhosis. To elucidate the pathological effect of H. pylori infection on the progression of hepatic fibrosis, C57BL/6 mice and Sprague-Dawley rats were orally inoculated with H. pylori, and hepatic fibrosis was induced with carbon tetrachloride (CCl 4 ) administration. We observed the histopathological changes and the presence of H. pylori genes by PCR in the liver. Significant increase in the fibrotic score as well as in serum alanine aminotransferase and aspartate aminotransferase levels was shown in the CCl 4 þ H. pylori group compared with that in the CCl 4 -treated group. Compared with the CCl 4 -treated group, a-smooth muscle actin and transforming growth factor-b1 were enhanced; however, senescence marker protein-30, a multifunctional protein protecting hepatocytes against oxidative stress and apoptosis, was suppressed in the CCl 4 þ H. pylori group. The 16S rRNA (400 bp) was demonstrated by PCR for H. pylori genes from genomic DNA extracted from the liver, and H. pylori-infected mice showed 93.8% (15 of 16) seropositivity by contrast with seronegativity in all H. pylori-noninfected mice. In addition, immunohistochemical study against H. pylori showed positive antigen fragments in the liver of the infected groups. Consequently, our data suggest that H. pylori infection could be an important contributing infectious factor to the development of liver cirrhosis.

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Section: Discussionsupporting

confidence: 60%

Section: Experimental Design-2mentioning

confidence: 99%

Helicobacter pylori promotes hepatic fibrosis in the animal model

Goo

Lee

et al. 2009

Laboratory Investigation

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“…To this end the extracts of KC (100 rtg protein/ml) were added to l0 s syngeneic bone marrow cells cultured in RPMI-1640 medium supplemented with 20% fetal calf serum, 2x10 -2 M 2-mercaptoethanol (for CFU-GM), L-glutamine (200 mg/liter), gentamicin (80 mg/liter), and 0.8% methylcellulose. Serum from anematized or zymosan-stimulated animals (for CFU-E and CFU-GM, respectively) was used as positive controls [3]. CFU-E consisting of no less than 50 cells were counted after 3 and CFU-GM after 7 days in culture at 37~ 5% CO:, and a humidified atmosphere in a CO:incubator (GPI-01, Leningrad).…”

Section: Methodsmentioning

confidence: 99%

Regulatory activity of Kupffer cells in acute blood loss

et al. 1995

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The scavenger function of Kupffer cells and the erythropoietinlike, granulocyte-macrophage colony-stimulating, and leukocyte-and lymphocyte-stimulating activities of extracts of Kupffer cells obtained before and at different times after acute massive blood loss were experimentally evaluated on mice. Extracts of Kupffer cells from normal mice are shown to exhibit all types of the studied activities. Acute blood loss reduces the scavenger function of Kupffer cells during the first few hours, especially erythropoietjnlike activity. The activities return to normal levels 5 days after blood loss and, after a relatively stable period, they rise again to the end of the recovery period. This is accompanied by an increase in the number of phagocytizing cells and is evidently related to the renewal of their population. Key Words: blood loss; hemopoiesis; Kupffer cellOutcomes of acute blood loss largely depend on the system of liver nonparenchymal cells, primarily Kupffer cells (KC), which are a component of the mononuclear phagocyte system responsible for the removal of old and partially destroyed erythrocytes [10]. It has been shown in our previous studies that prestimulation of the mononuclear phagocyte system with bacterial or yeast polysacchafides, prodigiosane or zymosan, 1-2 days prior to acute blood loss primarily hastened the recovery of erythron [2], while the corresponding potentiation of the granulocyte-macrophagal component of the bone marrow occurred later.Apart from their excellent capacity to scavenge erythrocytes, KC produce and secrete erythropoietin and other cytokines regulating hemopoiesis (interleukin-1, tumor necrosis factor-co -TNF-0c, granulocyte-macrophagal colony-stimulating factor, etc.) [8,12]. This function, normally weak, becomes markedly enhanced after partial hepatec- This suggests that KC also play a key role in the recovery of hemopoiesis after blood loss. However, their regenerative activity in this situation is poorly understood. In the present investigation we studied hemopoiesis-, leukocyte-, and lymphocytestimulating activities of KC in different phases of the posthemorrhagic period. MATERIALS AND METHODSThe experiments were carried out on 45 CBA mice of both sexes weighing 20-25 g. Blood (2.5% body weight) was drawn from the retroorbital sinus.Blood clearance from a colloid was determined as described earlier [6]. Colloid carbon (0.2 mg/g body weight, Gunter Wagner) was injected intravenously. The half-life and the rate constant of blood clearance from the colloid (C index, rain -1) were calculated from the curves. The mean number of KC with phagocytized carbon particles was determined on liver sections stained with hematoxylin and eosin at xl000 in 10 visual fields.

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“…In animals with CC14-induced liver cirrhosis, the ability of the blood system to respond to additional stimulating influences sharply decreases [3,8]. The number of progenitor cells, especially granulomonocytic precursors in the bone marrow decreased considerably.…”

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confidence: 99%

Growth-inhibitory activity of bone marrow cells during CCl4-induced liver cirrhosis

Zubakhin

Kutina

1999

Bull Exp Biol Med

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During CCl4-induced liver cirrhosis, cells of the hemopoiesis-inducing microenvironment in the bone marrow of BALB/c mice produced activity inhibiting the growth of erythropoiesis and granulomonocytopoiesis precursors. Stimulation with yeast polysaccharide zymosan increased the inhibitory activity (especially in relation to granulomonocytic precursors). The highest growth-inhibitory activity was produced by the bone marrow adherent fraction (residual bone marrow macrophages). Tumor necrosis factor-a is probably responsible for the inhibition of the growth of myeloid precursors in mice with CC14-induced liver cirrhosis.

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Functional state of the hematopoietic system in different stages of CCl4-induced liver fibrosis in mice

Cited by 3 publications

References 5 publications

Helicobacter pylori promotes hepatic fibrosis in the animal model

Helicobacter pylori promotes hepatic fibrosis in the animal model

Regulatory activity of Kupffer cells in acute blood loss

Growth-inhibitory activity of bone marrow cells during CCl4-induced liver cirrhosis

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