An ultrastructural study, effects of Proteus vulgaris OX19 on the rabbit spleen cells

Gül, Nursel; Özkorkmaz, Ebru Gökalp; Keleşoğlu, İlknur; Özlük, Aydın

doi:10.1016/j.micron.2012.05.010

Cited by 5 publications

(4 citation statements)

References 17 publications

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“…As previously described elsewhere (Gul et al, 2013), ileum tissues were immersed in 2% glutaraldehyde (pH 7.4) and chilled for 2 hours. After rinsing several times in cold sodium phosphate buffer, the tissues were then postfixed in 1% osmium tetroxide solution for 2 hours at 4°C.…”

Section: Methodsmentioning

confidence: 99%

Puerarin Ameliorates Experimental Alcoholic Liver Injury by Inhibition of Endotoxin Gut Leakage, Kupffer Cell Activation, and Endotoxin Receptors Expression

Peng

Cui

Huang

et al. 2012

J Pharmacol Exp Ther

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Puerarin, an isoflavone component extracted from Kudzu (Pueraria lobata), has been demonstrated to alleviate alcoholrelated disorders. Our study examined whether puerarin ameliorates chronic alcoholic liver injury through inhibition of endotoxin gut leakage, the subsequent Kupffer cell activation, and endotoxin receptors expression. Rats were provided with the Liber-DeCarli liquid diet for 8 weeks. Puerarin (90 mg/kg or 180 mg/kg daily) was orally administered from the beginning of the third week until the end of the experiment. Chronic alcohol intake caused increased serum alanine aminotransferase, aspartate aminotransferase, hepatic gamma-glutamyl transpeptidase, and triglyceride levels as well as fatty liver and neutrophil infiltration in hepatic lobules as determined by biochemical and histologic assays. A significant increase of liver tumor necrosis factor a was detected by enzyme-linked immunosorbent assay. These pathologic effects correlated with increased endotoxin level in portal vein and upregulated protein expression of hepatic CD68, lipopolysaccharide-binding protein, CD14, Toll-like receptor 2, and Toll-like receptor 4. Meanwhile, the intestinal microvilli were observed to be sparse, shortened, and irregularity in distribution under the transmission electron microscope in conjunction with the downregulated intestinal zonula occludens-1 protein expression. These hepatic pathologic changes were significantly inhibited in puerarintreated animals as were the endotoxin levels and hepatic CD68 and endotoxin receptors. Moreover, the pathologic changes in intestinal microvillus and the decreased intestinal zonula occludens-1 were also ameliorated with puerarin treatment. These results thus demonstrate that puerarin inhibition of endotoxin gut leakage, Kupffer cell activation, and endotoxin receptors expression is involved in the alleviation of chronic alcoholic liver injury in rats.

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Section: Methodsmentioning

confidence: 99%

Puerarin Ameliorates Experimental Alcoholic Liver Injury by Inhibition of Endotoxin Gut Leakage, Kupffer Cell Activation, and Endotoxin Receptors Expression

Peng

Cui

Huang

et al. 2012

J Pharmacol Exp Ther

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“…Splenic tissues were double fixed in 2.5% glutaraldehyde and 1% osmic acid for 2 h and then rapidly stained with 2% acetic acid U, dehydrated in a graded series of alcohol and acetone, embedded in Epon 812 and cut with a Reichert-Jung ultramicrotome. The specimens were double stained with acetic acid U and lead citrate solution and examined with a HITACHIH-7650 operating at 80 kV [ 36 ].…”

Section: Methodsmentioning

confidence: 99%

The diffuse reduction in spleen density: an indicator of severe acute pancreatitis?

et al. 2017

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We observed that acute pancreatitis (AP) was associated with diffuse reduction in spleen density (DROSD) in some patients. Furthermore, the condition of these patients was more serious, and the potential relationship between DROSD and structural and functional injury of the spleen remained unclear. Therefore, we performed a preliminary exploration of these factors. We analysed pertinent clinical data for AP patients with normal spleen density (control group) and for those with DROSD (reduction group) at the First Affiliated Hospital of Harbin Medical University (June 2013–June 2015). We measured the immunoglobulin M (IgM) B-cells of the AP patients and examined pancreatic and splenic tissues from AP rats with optical microscopy and TEM. The reduction group had a higher acute physiology and chronic health evaluation II (APACHE II) score, a longer length of stay (LOS) and lower serum calcium than the control group. The levels of triglycerides (TG) and total cholesterol (TC) did not differ significantly between the two groups. The percentage of IgM memory B-cells was significantly lower in the DROSD group than in the control group. TEM revealed that the spleen T-lymphocytes were normal in AP rats, but pyroptotic and necrotic spleen B-cells were observed in the severe AP rats. In AP, DROSD was an independent indicator of more severe conditions. Furthermore, spleen B-lymphocytes showed obvious damage at the cellular level, and the immunological function of the spleen was down-regulated when AP was associated with DROSD.

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“…Preparation of pathological slices from samples of fixed mouse brain was carried out according to previous reports ( 13 , 16 ). In brief, about 2 mm 3 of brain samples for TEM were immersed in 2.5% glutaraldehyde buffer (pH 7.4 with 0.1 M sodium phosphate) and kept at 4°C for more than 24 h, and then washed three times in cold sodium phosphate buffer.…”

Section: Methodsmentioning

confidence: 99%

Exploration of the main sites for the transformation of normal prion protein (PrP^C) into pathogenic prion protein (PrP^sc)

Feng

Wang

et al. 2017

Journal of Veterinary Research

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IntroductionThe functions and mechanisms of prion proteins (PrPC) are currently unknown, but most experts believe that deformed or pathogenic prion proteins (PrPSc) originate from PrPC, and that there may be plural main sites for the conversion of normal PrPC into PrPSc. In order to better understand the mechanism of PrPC transformation to PrPSc, the most important step is to determine the replacement or substitution site.Material and MethodsBALB/c mice were challenged with prion RML strain and from 90 days post-challenge (dpc) mice were sacrificed weekly until all of them had been at 160 dpc. The ultra-structure and pathological changes of the brain of experimental mice were observed and recorded by transmission electron microscopy.ResultsThere were a large number of pathogen-like particles aggregated in the myelin sheath of the brain nerves, followed by delamination, hyperplasia, swelling, disintegration, phagocytic vacuolation, and other pathological lesions in the myelin sheath. The aggregated particles did not overflow from the myelin in unstained samples. The phenomenon of particle aggregation persisted all through the disease course, and was the earliest observed pathological change.ConclusionIt was deduced that the myelin sheath and lipid rafts in brain nerves, including axons and dendrites, were the main sites for the conversion of PrPC to PrPSc, and the PrPSc should be formed directly by the conversion of protein conformation without the involvement of nucleic acids.

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An ultrastructural study, effects of Proteus vulgaris OX19 on the rabbit spleen cells

Cited by 5 publications

References 17 publications

Puerarin Ameliorates Experimental Alcoholic Liver Injury by Inhibition of Endotoxin Gut Leakage, Kupffer Cell Activation, and Endotoxin Receptors Expression

Puerarin Ameliorates Experimental Alcoholic Liver Injury by Inhibition of Endotoxin Gut Leakage, Kupffer Cell Activation, and Endotoxin Receptors Expression

The diffuse reduction in spleen density: an indicator of severe acute pancreatitis?

Exploration of the main sites for the transformation of normal prion protein (PrP^C) into pathogenic prion protein (PrP^sc)

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An ultrastructural study, effects of Proteus vulgaris OX19 on the rabbit spleen cells

Cited by 5 publications

References 17 publications

Puerarin Ameliorates Experimental Alcoholic Liver Injury by Inhibition of Endotoxin Gut Leakage, Kupffer Cell Activation, and Endotoxin Receptors Expression

Puerarin Ameliorates Experimental Alcoholic Liver Injury by Inhibition of Endotoxin Gut Leakage, Kupffer Cell Activation, and Endotoxin Receptors Expression

The diffuse reduction in spleen density: an indicator of severe acute pancreatitis?

Exploration of the main sites for the transformation of normal prion protein (PrPC) into pathogenic prion protein (PrPsc)

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Product

Resources

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Exploration of the main sites for the transformation of normal prion protein (PrP^C) into pathogenic prion protein (PrP^sc)