• Title/Summary/Keyword: Hepatic inflammation

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Clinical and Histopathogical Studies of Experimentally Induced Listeriosis in Korean Native Goats (한국재래산양의 Listeria병에 관한 임상 및 병리조직학적 연구)

  • Kwak Soo-Dong;Yeo Sang-Geon
    • Journal of Veterinary Clinics
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    • v.5 no.1
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    • pp.43-52
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    • 1988
  • These studies were taken experimentally to clarify the clinical and histopathological findings of listeriosis in Korean native goat(KNC). Four KNGs of 4 to 5 months of age were inoculated orally or in-travenously (IV) with Listeria monocytogenes isolated from a field case of KNG. 1. On the clinical findings, depression, anorexia and fever were observed in all inoculated goats, and nasal discharge, keratoconjunctivitis and diarrhea in 3 of 4 goats. Highest rectal temperature after in-oculation was 2.5$^{\circ}C$ higher in IV inoculated goats and 1.9$^{\circ}C$ higher in orally inoculated than normal rectal temperature observed before inoculation. Durations of clinical course after inoculation in IV and orally inoculated goats were 5 days and 8 days, respectively. 2. On the gross lesions, swelling of the lymph nodes, hemorrhage and .inflammation of the small intestine and rigor mortis were observed in 4 of 4 goats, and keratoconjunctivitis, hemorrhage and inflammation of the large intestine, swelling of the spleen, pneumonia and hydropericardium in 3 of 4 goats. Congestion of the visceral organs and ecchymosis of the sin in a fetus were observed. Keratoconjunctivitis, hemorrhage of the abomasum, swelling of the lymph node, hemorrhage and inflammation of the small intestine, swelling of the spleen, necrosis of the liver and pneumonia were observed as severe lesions. These lesions were more severe in IV inoculated goats than those in orally inoculated goats. 3. On histopathological findings, focal necrosis found throughout the livers occurred mainly on peripheral areas of hepatic lobules. These necrotic foci consisted of neutrophils, lymphocytes, macrophages, short rod bacteria and necretic hepatic cells. Suppurative pneumonia of the lung, hyperemia, congestion, epithelial necrosis and sloughing of the small and large intestine, swelling in periventricular regions of the central nervous system, swelling of the kidney, spleen and lymph node were observed as listerial lesions.

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Porphyromonas gingivalis exacerbates the progression of fatty liver disease via CD36-PPARγ pathway

  • Ahn, Ji-Su;Yang, Ji Won;Oh, Su-Jeong;Shin, Ye Young;Kang, Min-Jung;Park, Hae Ryoun;Seo, Yoojin;Kim, Hyung-Sik
    • BMB Reports
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    • v.54 no.6
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    • pp.323-328
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    • 2021
  • Periodontal diseases have been reported to have a multidirectional association with metabolic disorders. We sought to investigate the correlation between periodontitis and diabetes or fatty liver disease using HFD-fed obese mice inoculated with P. gingivalis. Body weight, alveolar bone loss, serological biochemistry, and glucose level were determined to evaluate the pathophysiology of periodontitis and diabetes. For the evaluation of fatty liver disease, hepatic nonalcoholic steatohepatitis (NASH) was assessed by scoring steatosis, inflammation, hepatocyte ballooning and the crucial signaling pathways involved in liver metabolism were analyzed. The C-reactive protein (CRP) level and NASH score in P. gingivalis-infected obese mice were significantly elevated. Particularly, the extensive lobular inflammation was observed in the liver of obese mice infected with P. gingivalis. Moreover, the expression of metabolic regulatory factors, including peroxisome proliferator-activated receptor γ (Pparγ) and the fatty acid transporter Cd36, was up-regulated in the liver of P. gingivalis-infected obese mice. However, inoculation of P. gingivalis had no significant influence on glucose homeostasis, insulin resistance, and hepatic mTOR/AMPK signaling. In conclusion, our results indicate that P. gingivalis can induce the progression of fatty liver disease in HFD-fed mice through the upregulation of CD36-PPARγ axis.

Attenuation of Anemia by Relmα in LPS-Induced Inflammatory Response

  • Lee, Mi-Ran
    • Journal of the Korea Society of Computer and Information
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    • v.23 no.10
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    • pp.135-141
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    • 2018
  • In this paper, we propose to evaluate the effect of resistin-like molecule alpha ($Relm{\alpha}$) on the progression of anemia of inflammation. Anemia of inflammation is a common feature of inflammatory disorders, including chronic kidney disease, infections, and rheumatoid arthritis. $Relm{\alpha}$ is highly up-regulated in various inflammatory states, especially those involving asthma, intestinal inflammation, and parasitic diseases, and regulates the pathogenesis of those diseases. However, the role of $Relm{\alpha}$ in anemia of inflammation is unknown. To explore the roles of $Relm{\alpha}$ in anemia of inflammation in vivo, we generated mouse model of the disease by injecting 0.25 mg/kg lipopolysaccharides (LPS) intraperitoneally into $Relm{\alpha}-deficient$ and wild-type (WT) mice daily for 10 days. Research data was expressed as differences between LPS-treated $Relm{\alpha}-deficient$ and WT mice by a two-tailed non-parametric Mann-Whitney U-test using GraphPad Instat program. The results of the study are as follows: LPS-treated $Relm{\alpha}-deficient$ mice had significantly (p<0.05) lower hemoglobin contents, hematocrit levels and red blood cell indices including mean corpuscular volume, mean corpuscular hemoglobin than WT controls. This decrease was accompanied by significant (p<0.05) increase in total white blood cell and monocyte counts in the blood. However, there was no significant difference in mRNA levels of hepatic hepcidin and renal erythropoietin between the two animal groups. Taken together, these results indicates that $Relm{\alpha}$ deficiency exacerbates the anemia by increasing inflammation, suggesting therapeutic value of $Relm{\alpha}$ in the treatment of anemia of inflammation.

Ursodeoxycholic acid decreases age-related adiposity and inflammation in mice

  • Oh, Ah-Reum;Bae, Jin-Sik;Lee, Junghoon;Shin, Eunji;Oh, Byung-Chul;Park, Sang-Chul;Cha, Ji-Young
    • BMB Reports
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    • v.49 no.2
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    • pp.105-110
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    • 2016
  • Ursodeoxycholic acid (UDCA), a natural, hydrophilic nontoxic bile acid, is clinically effective for treating cholestatic and chronic liver diseases. We investigated the chronic effects of UDCA on age-related lipid homeostasis and underlying molecular mechanisms. Twenty-week-old C57BL/6 male and female mice were fed a diet with or without 0.3% UDCA supplementation for 25 weeks. UDCA significantly reduced weight gain, adiposity, hepatic triglyceride, and hepatic cholesterol without incidental hepatic injury. UDCA-mediated hepatic triglyceride reduction was associated with downregulated hepatic expression of peroxisome proliferator-activated receptor-γ, and of other genes involved in lipogenesis (Chrebp, Acaca, Fasn, Scd1, and Me1) and fatty acid uptake (Ldlr, Cd36). The inflammatory cytokines Tnfa, Ccl2, and Il6 were significantly decreased in liver and/or white adipose tissues of UDCA-fed mice. These data suggest that UDCA exerts beneficial effects on age-related metabolic disorders by lowering the hepatic lipid accumulation, while concurrently reducing hepatocyte and adipocyte susceptibility to inflammatory stimuli.

The Effect of Dietary Docosahexaenoic Acid Enrichment on the Expression of Porcine Hepatic Genes

  • Chang, W.C.;Chen, C.H.;Cheng, W.T.K.;Ding, S.T.
    • Asian-Australasian Journal of Animal Sciences
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    • v.20 no.5
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    • pp.768-774
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    • 2007
  • To study the effect of dietary docosahexaenoic acid (DHA) enrichment on the expression of hepatic genes in pigs, weaned, crossbred pigs (30 d old) were fed diets supplemented with either 2% tallow or DHA oil for 18 d. Hepatic mRNA was extracted. Suppression subtractive hybridization was used to explore the hepatic genes that were specifically regulated by dietary DHA enrichment. After subtraction, we observed 288 cDNA fragments differentially expressed in livers from pigs fed either 2% DHA oil or 2% tallow for 18 d. After differential screening, 7 genes were found to be differentially expressed. Serum amyloid A protein 2 (SAA2) was further investigated because of its role in lipid metabolism. Northern analysis indicated that hepatic SAA2 was upregulated by dietary DHA enrichment (p<0.05). In a second experiment, feeding 10% DHA oil for 2d significantly increased the expression of SAA2 (compared to the 10% tallow group; p<0.05). The porcine SAA2 full length cDNA sequence was cloned and the sequence was compared to the human and mouse sequences. The homology of the SAA2 amino acid sequence between pig and human was 73% and between pig and mouse was 62%. There was a considerable difference in SAA2 sequences among these species. Of particular note was a deletion of 8 amino acids, in the pig compared to the human. This fragment is a specific characteristic for the SAA subtype that involved in acute inflammation reaction. Similar to human and mouse, porcine SAA2 was highly expressed in the liver of pigs. It was not detectable in the skeletal muscle, heart muscle, spleen, kidney, lung, and adipose tissue. These data suggest that SAA2 may be involved in mediation of the function of dietary DHA in the liver of the pig, however, the mechanism is not yet clear.

The Antifibrotic Effects of Polysaccharides Extracted from Garnoderma lucidum on the Experimental Hepatic Cirrhosis (영지로부터 추출한 다당체의 실험적 간경화에 대한 섬유화 억제효과)

  • Park, Eun-Jeon;Kim, Ki-Young;Kim, Jae-Baek;Kim, Soo-Woong;Lee, Seung-Yong;Sohn, Dong-Hwan
    • YAKHAK HOEJI
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    • v.38 no.3
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    • pp.338-344
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    • 1994
  • This study was carried out to investigate the antifibrotic effects of polysaccharides extracted from Garnoderma lucidum. The biliary cirrhosis was induced by bile duct ligation/scission (BDL/S) in rats. BDL/S rats were dosed 5 mg/rat/day orally for 4 weeks after the operation. Antifibrotic effects were evaluated by serum biochemical values, serum procollagen type III peptide (PIIINP) levels, liver hydroxyproline contents, and light microscopical histology. The results obtained were as follows; 1) PIIINP levels in sera of treated BDL/S group were lowered to 50% of those of untreated BDL/S group. 2) Hydroxyproline contents in the liver of treated BDL/S group were also reduced to 83% of those of untreated BDL/S rats. 3) The hepatic damage such as hepatocellular necrosis, inflammation, bile duct proliferation and fibrosis was less severe in the livers of treated rats. These results suggest polysaccharides extracted from Garnoderma lucidum to be a promising agent for the inhibition of hepatic cirrhosis(fibrosis).

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Role of Kupffer Cells in Vasoregulatory Gene Expression During Endotoxemia

  • Kim, Tae-Hoon;Lee, Sun-Mee
    • Biomolecules & Therapeutics
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    • v.16 no.4
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    • pp.306-311
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    • 2008
  • Although hepatic microcirculatory dysfunction occurs during endotoxemia, the mechanism responsible for this remains unclear. Since Kupffer cells provide signals that regulate hepatic response in inflammation, this study was designed to investigate the role of Kupffer cells in the imbalance in the expression of vasoactive mediators. Endotoxemia was induced by intraperitoneal E. coli endotoxin (LPS, 1 mg/kg body weight). Kupffer cells were inactivated with gadolinium chloride ($GdCl_3$, 7.5 mg/kg body weight, intravenously) 2 days prior to LPS exposure. Liver samples were taken 6 h following LPS exposure for RT-PCR analysis of mRNA for genes of interest: endothelin (ET-1), its receptors $ET_A$ and $ET_B$, inducible nitric oxide synthase (iNOS), heme oxygenase (HO-1), and tumor necrosis factor-$\alpha$ (TNF-$\alpha$). mRNA levels for iNOS and TNF-$\alpha$ were significantly increased 31.8-fold and 26.7-fold in LPS-treated animals, respectively. This increase was markedly attenuated by $GdCl_3$, HO-1 expression significantly increased in LPS-treated animals, with no significant difference between saline and $GdCl_3$ groups. ET-1 was increased by LPS. mRNA levels for $ET_A$ receptor showed no change, whereas $ET_B$ transcripts increased in LPS-treated animals. The increase in $ET_B$ transcripts was potentiated by $GdCl_3$. We conclude that activation of Kupffer cells plays an important role in the imbalanced hepatic vasoregulatory gene expression induced by endotoxin.

The Cone (Pinus densiflora) Induced Apoptosis and Autophagy in Hepatic Stellate Cells

  • Tae-Won Jang;Da-Yoon Lee;So-Yeon Han;Hye-Jeong Park;Seo-Yoon Park;Jun-Hwan Jeong;Yoon-Jae Kwon;Jae-Ho Park
    • Proceedings of the Plant Resources Society of Korea Conference
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    • 2022.09a
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    • pp.106-106
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    • 2022
  • The cone of Red Pine (Pinus densiflora), which has been used as a drug in traditional medicine. Its ethyl acetate fraction was reported to exert antioxidant, anti-melanogenesis, and anti-inflammation activites. Apoptosis of hepatic stellate cells (LX-2) is regarding as a potential strategy for alleviation of hepatic fibrosis. We conducted to investigated whether the treatment of cone has a potential to control of some factors related in apoptosis and autophagy in cell signaling pathways. We suggest that the cone induced apoptosis through confirming the expression levels of genes (cPARP, Bcl-XL, Bax, p53, and caspase-3) in LX-2 cells. Also, the cone may regulate autophagy (LC3, p62, Beclin-1, and ATG12). Remarkably, the treatment of cone may affect to formation of autophagosomes in the immunofluorescence image in live cells. These findings suggest that the ethyl acetate fraction from the cone of Red Pine (P. densiflora) may have potential as an alternative therapeutic agent for the alleviation and prevention of liver fibrosis.

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Mentha canadensis attenuates adiposity and hepatic steatosis in high-fat diet-induced obese mice

  • Youngji Han;Ji-Young Choi;Eun-Young Kwon
    • Nutrition Research and Practice
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    • v.17 no.5
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    • pp.870-882
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    • 2023
  • BACKGROUND/OBJECTIVES: Obesity is a major risk factor for metabolic syndrome, a global public health problem. Mentha canadensis (MA), a traditional phytomedicine and dietary herb used for centuries, was the focus of this study to investigate its effects on obesity. MATERIALS/METHODS: Thirty-five male C57BL/6J mice were randomly divided into 2 groups and fed either a normal diet (ND, n = 10) or a high-fat diet (HFD, n = 25) for 4 weeks to induce obesity. After the obesity induction period, the HFD-fed mice were randomly separated into 2 groups: one group continued to be fed HFD (n = 15, HFD group), while the other group was fed HFD with 1.5% (w/w) MA ethanol extract (n = 10, MA group) for 13 weeks. RESULTS: The results showed that body and white adipose tissue (WAT) weights were significantly decreased in the MA-supplemented group compared to the HFD group. Additionally, MA supplementation enhanced energy expenditure, leading to improvements in plasma lipids, cytokines, hepatic steatosis, and fecal lipids. Furthermore, MA supplementation regulated lipid-metabolism-related enzyme activity and gene expression, thereby suppressing lipid accumulation in the WAT and liver. CONCLUSIONS: These findings indicate that MA has the potential to improve diet-induced obesity and its associated complications, including adiposity, dyslipidemia, hepatic steatosis, and inflammation.

Effect of Oligonol, a Low Molecular Weight Polyphenol Derived from Lychee on Oxidative Stress-Related Hepatic Damage in Streptozotocin-Induced Diabetic Rats (리치 저분자 폴리페놀인 Oligonol의 Streptozotocin 투여 당뇨 쥐에서 산화적 스트레스와 관련된 간 손상에 미치는 영향)

  • Noh, Jeong Sook
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.44 no.4
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    • pp.475-482
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    • 2015
  • This study was conducted to examine whether or not oligonol, a low molecular weight polyphenol derived from lychee fruit, has an ameliorative effect on diabetes-induced oxidative stress-related hepatic damage in streptozotocin (STZ)-induced diabetic rats. Oligonol (10 or 20 mg/kg body weight; O10 or O20, respectively) was orally administered every day for 10 days to STZ-induced diabetic rats, and its effects were compared to vehicle-treated diabetic (Veh) and non-diabetic rats. Administration of 20 mg/kg of oligonol significantly decreased liver weight compared with the Veh group (P<0.05). Elevated levels of hepatic glucose, reactive oxygen species, peroxynitrite, and lipid peroxidation were detected in diabetic vehicle rats, whereas oligonol treatment significantly attenuated these levels (P<0.05). In diabetic vehicle rats, hepatic antioxidant enzyme protein levels decreased, whereas oligonol treatment showed significant elevated results. For inflammation-related protein expression, oligonol-treated groups showed insignificant reduction. Oligonol improved expression of proapoptotic protein caspase-3 in the liver of diabetic rats (P<0.05). In conclusion, these results provide important evidence that oligonol exhibits an inhibitory effect on oxidative stress and apoptosis-related protein expression as well as a hepato-protective effect against the development of diabetic complications in STZ-induced type 1 diabetic rats.