• Biomedical Science Letters
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• v.12 no.4
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• pp.355-359
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• 2006

This investigation was performed to study the antioxidant activities of Cornus officinalis Sieb extracts and the effect of Cornus officinalis Sieb extracts on glucose, lipid metabolism in diabetic rats. DPPH free radical scavanging activity and superoxide anion radical scavenging of Cornus officinalis Sieb extracts were 94.7% and 92.1%, respectively. Streptozotocin (45 mg/kg body weight, i.p.) induced diabetic rats showed a significant increases of plasma glucose, triglyceride and total cholesterol, concomitantly significant decrease of plasma high density lipoprotein. Glutathione level were decrease in cytosol of liver, lung and brain tissue of rats. Lipid peroxide were increase in microsome of liver cells. Group 1 and 2 were treated with Cornus officinalis Sieb extracts 200 mg/kg body weight and 100 mg/kg body weight for 24 days, individually. Group 1 and 2 rats showed decreased plasma glucose, triglyceride, total cholesterol and lipid peroxide in microsome of liver, and increased plasma high density lipoprotein and glutathione in cytosol of liver, lung and brain. The result suggest that Cornus officinalis Sieb extracts may normalize the Impaired antioxiants status in streptozotocin induced diabetic rats. Cornus officinalis Sieb extracts were used to improve the imbalance between free radicals and antioxidant system due to the diabetes.

• Korean Journal of Rural Living Science
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• v.5 no.2
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• pp.125-134
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• 1994

This study was performed to observe the effects of dietary fat levels and sources on lipids contents and cellularities of liver, brain, and adipose tissue of early weaned rats. Male Sprague-Dawley rats were prematurely weaned from postnatal 17th day with the experimental diets differ in fat levels : low(5%), medium(10%), high(20%) and fat sources : butter, soybean oil, butter＋ soybean oil. On the postnatal 29th day, contents of total lipid, triglyceride, cholesterol and phospholipid of serum, liver, brain and adipose tissue were determined, and DNA was determined to assess the cell growth. Rats early weaned fed high fat diet showed lower total lipid and triglyceride levels in serum and liver than those fed medium or low fat diet Rats early weaned fed high fat diet had adipocytes of fewer number, but larger size than those of rats fed low or medium fat diets. Rats early weaned fed soybean oil diet had more adipocytes thu those fed butter diet. Rats normally weaned to commercial chow diet showed lower total lipid, triglyceride, and cholesterol levels in serum and liver, had fewer adipocytes than all early weaned rats except for rats fed high fat-butter diet. These results suggest that high fat-butter diet is ideal weaning diet at early weaning.

• Korean Journal of Radiology
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• v.21 no.8
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• pp.987-997
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• 2020

Objective: Measurement of the liver and spleen volumes has clinical implications. Although computed tomography (CT) volumetry is considered to be the most reliable noninvasive method for liver and spleen volume measurement, it has limited application in clinical practice due to its time-consuming segmentation process. We aimed to develop and validate a deep learning algorithm (DLA) for fully automated liver and spleen segmentation using portal venous phase CT images in various liver conditions. Materials and Methods: A DLA for liver and spleen segmentation was trained using a development dataset of portal venous CT images from 813 patients. Performance of the DLA was evaluated in two separate test datasets: dataset-1 which included 150 CT examinations in patients with various liver conditions (i.e., healthy liver, fatty liver, chronic liver disease, cirrhosis, and post-hepatectomy) and dataset-2 which included 50 pairs of CT examinations performed at ours and other institutions. The performance of the DLA was evaluated using the dice similarity score (DSS) for segmentation and Bland-Altman 95% limits of agreement (LOA) for measurement of the volumetric indices, which was compared with that of ground truth manual segmentation. Results: In test dataset-1, the DLA achieved a mean DSS of 0.973 and 0.974 for liver and spleen segmentation, respectively, with no significant difference in DSS across different liver conditions (p = 0.60 and 0.26 for the liver and spleen, respectively). For the measurement of volumetric indices, the Bland-Altman 95% LOA was -0.17 ± 3.07% for liver volume and -0.56 ± 3.78% for spleen volume. In test dataset-2, DLA performance using CT images obtained at outside institutions and our institution was comparable for liver (DSS, 0.982 vs. 0.983; p = 0.28) and spleen (DSS, 0.969 vs. 0.968; p = 0.41) segmentation. Conclusion: The DLA enabled highly accurate segmentation and volume measurement of the liver and spleen using portal venous phase CT images of patients with various liver conditions.

• Parasites, Hosts and Diseases
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• v.62 no.2
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• pp.243-250
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• 2024

We investigated organ specific Toxocara canis larval migration in mice infected with T. canis larvae. We observed the worm burden and systemic immune responses. Three groups of BALB/c mice (n=5 each) were orally administered 1,000 T. canis 2nd stage larvae to induce larva migrans. Mice were sacrificed at 1, 3, and 5 weeks post-infection. Liver, lung, brain, and eye tissues were collected. Tissue from 2 mice per group was digested for larval count, while the remaining 3 mice underwent histological analysis. Blood hematology and serology were evaluated and compared to that in a control uninfected group (n=5) to assess the immune response. Cytokine levels in bronchoalveolar lavage (BAL) fluid were also analyzed. We found that, 1 week post-infection, the mean parasite load in the liver (72±7.1), brain (31±4.2), lungs (20±5.7), and eyes (2±0) peaked and stayed constant until the 3 weeks. By 5-week post-infection, the worm burden in the liver and lungs significantly decreased to 10±4.2 and 9±5.7, respectively, while they remained relatively stable in the brain and eyes (18±4.2 and 1±0, respectively). Interestingly, ocular larvae resided in all retinal layers, without notable inflammation in outer retina. Mice infected with T. canis exhibited elevated levels of neutrophils, monocytes, eosinophils, and immunoglobulin E. At 5 weeks post-infection, interleukin (IL)-5 and IL-13 levels were elevated in BAL fluid. Whereas IL-4, IL-10, IL-17, and interferon-γ levels in BAL fluid were similar to that in controls. Our findings demonstrate that a small portion of T. canis larvae migrate to the eyes and brain within the first week of infection. Minimal tissue inflammation was observed, probably due to increase of anti-inflammatory cytokines. This study contributes to our understanding of the histological and immunological responses to T. canis infection in mice, which may have implications to further understand human toxocariasis.

• Korean Journal of Veterinary Service
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• v.16 no.1
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• pp.57-64
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• 1993

This survey was performed to report rare outbreak of liver cirrhosis in Korean native goat (KNG) which was died of Yangpyeong's goat farm on Feb. 1992. The examination for the KNG was carried out by clinical signs, necropsy and various lab-oratory test including parasitic, bacterial and histological test. The KNG looked jaundice, ascite, hemorrhage of lumen, abomasum and intestine, and brownish smooth cirrhotic liver at necropsy. Histological examination for liver revealed considerable proliferation of connective tissue and piecemeal necrosis which was caused by chronic active inflammation in interlobules and intralobules. There were atrophic micro and macro nodules which were sur-rounded by connective tissue. The lobular structure lack almost all central vein. The portal areas appearred proliferation of bile ducts, blood vessels and connective tissues. These connective tissue infiltrated heavily with plasma cells, Iymphocytes and histocytes. Histological examination for brain proved to be hepatic encephalopathy by virture of congestion and edema in cerebral medullary. From these results were demonstrated miked nodular, active, postnecrotic liver cirrhosis.

• Toxicological Research
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• v.30 no.4
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• pp.243-250
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• 2014

Mitochondrial integrity is critical for maintaining proper cellular functions. A key aspect of regulating mitochondrial homeostasis is removing damaged mitochondria through autophagy, a process called mitophagy. Autophagy dysfunction in various disease states can inactivate mitophagy and cause cell death, and defects in mitophagy are becoming increasingly recognized in a wide range of diseases from liver injuries to neurodegenerative diseases. Here we highlight our current knowledge on the mechanisms of mitophagy, and discuss how alterations in mitophagy contribute to disease pathogenesis. We also discuss mitochondrial dynamics and potential interactions between mitochondrial fusion, fission and mitophagy.

• Journal of Food Hygiene and Safety
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• v.17 no.3
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• pp.124-128
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• 2002

The effect of different ethanol feeding protocols on the oxidative stress in liver and blain of rats was studied. The rats were fed 5%-ethanol solution in drinking water (5%-EtOH group) or 2.5g ethanol/kg body wt. once daily intragastrically (2.5g-EtOH group). The levels of thiobarbituric acid reactive substances (TRARS) and vitamin EI in the liver, cerebrum and cerebellum were measured. In the liver of 5%-EtOH group, the level of TBARS was not changed, whereas vitamin I was significantly increased compared to control group. In the liver of 2.5g-EtOH group, the level of TBARS was significantly increased compared to control group and the vitamin E concentration was not affected. The levels of TBARS were increased and the vitamin E concentrations were decreased significantly both in the cerebrum and cerebellum in 5%-EtOH group as well as in 2.5g-EtOH group. These results show that lipid peroxidation and vitamin E concentration in liver were varied according to the conditions of ethanol treatment, however, the vitamin E contents in cerebrum and cerebellum were affected by both ethanol intoxications used in this study.

• Toxicological Research
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• v.31 no.4
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• pp.347-354
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• 2015

Excess manganese (Mn) is neurotoxic. Increased manganese stores in the brain are associated with a number of behavioral problems, including motor dysfunction, memory loss and psychiatric disorders. We previously showed that the transport and neurotoxicity of manganese after intranasal instillation of the metal are altered in Hfe-deficient mice, a mouse model of the iron overload disorder hereditary hemochromatosis (HH). However, it is not fully understood whether loss of Hfe function modifies Mn neurotoxicity after ingestion. To investigate the role of Hfe in oral Mn toxicity, we exposed Hfe-knockout ($Hfe^{-/-}$) and their control wild-type ($Hfe^{+/+}$) mice to $MnCl_2$ in drinking water (5 mg/mL) for 5 weeks. Motor coordination and spatial memory capacity were determined by the rotarod test and the Barnes maze test, respectively. Brain and liver metal levels were analyzed by inductively coupled plasma mass spectrometry. Compared with the water-drinking group, mice drinking Mn significantly increased Mn concentrations in the liver and brain of both genotypes. Mn exposure decreased iron levels in the liver, but not in the brain. Neither Mn nor Hfe deficiency altered tissue concentrations of copper or zinc. The rotarod test showed that Mn exposure decreased motor skills in $Hfe^{+/+}$ mice, but not in $Hfe^{-/-}$ mice (p = 0.023). In the Barns maze test, latency to find the target hole was not altered in Mn-exposed $Hfe^{+/+}$ compared with water-drinking $Hfe^{+/+}$ mice. However, Mn-exposed $Hfe^{-/-}$ mice spent more time to find the target hole than Mn-drinking $Hfe^{+/+}$ mice (p = 0.028). These data indicate that loss of Hfe function impairs spatial memory upon Mn exposure in drinking water. Our results suggest that individuals with hemochromatosis could be more vulnerable to memory deficits induced by Mn ingestion from our environment. The pathophysiological role of HFE in manganese neurotoxicity should be carefully examined in patients with HFE-associated hemochromatosis and other iron overload disorders.

• Journal of the Korean Society of Food Science and Nutrition
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• v.20 no.5
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• pp.418-425
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• 1991

This study was designed to observe the effects of the fish oil and some seed oils on the improvement of the fatty acid compositions of liver and brain tissue in rats. In order to induce the hypertriglyceridemia in the rats of the Sprague-Dawley, 12% coconut oil and 3% each of olive oil, lard, fish oil, perilla oil, corn oil, red pepper seed oil and evening primrose oil were administered to the rats for 4 weeks. In the fatty acid composition of liver lipid, n-3 PUFA contents were most in the fish oil and perilla oil groups of phospholipid fraction, and n-6 PUFA contents were most in the corn oil, red pepper seed oil and evening primrose oil groups of triglyceride fractions. Fatty acid composition of liver lipid fractions were influenced from the fatty acid composition of the test lipids. In the fatty acid composition of brain phospholipid, n-3 PUFA contents (8.8~17.2%) were most in the fish oil group, and n-6 PUFA (34.6~38.2%), though it contains high percentage, showed little difference between groups.

• BMB Reports
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• v.42 no.8
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• pp.475-481
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• 2009

Emerging data demonstrate pivotal roles for brain insulin resistance and insulin deficiency as mediators of cognitive impairment and neurodegeneration, particularly Alzheimer's disease (AD). Insulin and insulin-like growth factors (IGFs) regulate neuronal survival, energy metabolism, and plasticity, which are required for learning and memory. Hence, endogenous brain-specific impairments in insulin and IGF signaling account for the majority of AD-associated abnormalities. However, a second major mechanism of cognitive impairment has been linked to obesity and Type 2 diabetes (T2DM). Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death. In essence, there are dual mechanisms of brain insulin resistance leading to AD-type neurodegeneration: one mediated by endogenous, CNS factors; and the other, peripheral insulin resistance with excess cytotoxic ceramide production.