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RISS 인기검색어
- 검색키워드
- 저자 : Hyeneui Jeong (검색결과 5 건)
- 무료
- 기관 내 무료
- 유료
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Jeong, Hyeneui,Kim, Jong-Won,Yang, Myeon-Sik,Park, Chul,Kim, Jong Hoon,Lim, Chae Woong,Kim, Bumseok World Scientific Publishing Company 2018 The American journal of Chinese medicine Vol.46 No.7
<P>Korean red ginseng (KRG) is a traditional herbal medicine used to prevent several geriatric diseases due to its therapeutic effects on metabolic disorder, including type 2 diabetes and fatty liver disease. In this study, we investigated the effects of KRG on the progression of nonalcoholic steatohepatitis (NASH) in mice. NASH was induced by feeding a methionine- and choline-deficient high-fat or high-fat/high-sucrose diet for 6 or 13 weeks, respectively. Each diet group was also orally administered saline (group G0) or KRG extract (100, 200, or 400 mg/kg/day; groups G1, G2, and G4, respectively). KRG showed anti-inflammatory and antifibrogenic effects in the diet-induced NASH models. Furthermore, the expression levels of lipid metabolism-related genes were markedly decreased with KRG treatment in both diet-induced NASH groups. We next confirmed the expression levels of FABP4 in the liver and its ability to regulate inflammation and/or oxidative stress. We observed decreased levels of FABP4 mRNA and protein in the KRG-treated groups indicating that KRG affects the pathogenesis of NASH-related inflammatory responses by modulating FABP4 expression. Results of <I>in vitro</I> experiments showed similar patterns in cells treated with KRG, indicating that KRG treatment regulates the expression of FABP4 and subsequently reduces NASH related inflammation. Our findings suggest a novel role of KRG in NASH-related inflammatory responses via modulation of FABP4 expression in the liver. KRG may be a safe alternative therapy to prevent NASH progression.</P>
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최나은,김종원,Hyeneui Jeong,신동구,서정헌,김종훈,임채웅,한강민,김범석 고려인삼학회 2019 Journal of Ginseng Research Vol.43 No.2
Background: Nonalcoholic steatohepatitis (NASH) is one of the chronic inflammatory liver diseases and a leading cause of advanced liver fibrosis, cirrhosis, and hepatocellular carcinoma. The main purpose of this study was to clarify the effects of GBCK25 fermented by Saccharomyces servazzii GB-07 and pectinase, on NASH severity in mice. Methods: Six-wk-old male mice were fed either a normal diet (ND) or a Western diet (WD) for 12 wks to induce NASH. Each group was orally administered with vehicle or GBCK25 once daily at a dose of 10 mg/ kg, 20 mg/kg, 100 mg/kg, 200 mg/kg, or 400 mg/kg during that time. The effects of GBCK25 on cellular damage and inflammation were determined by in vitro experiments. Results: Histopathologic analysis and hepatic/serum biochemical levels revealed that WD-fed mice showed severe steatosis and liver injury compared to ND-fed mice. Such lesions were significantly decreased in the livers of WD-fed mice with GBCK25 administration. Consistently, mRNA expression levels of NASH-related inflammatory-, fibrogenic-, and lipid metabolism-related genes were decreased in the livers of WD-fed mice administered with GBCK25 compared to WD-fed mice. Western blot analysis revealed decreased protein levels of cytochrome P450 2E1 (CYP2E1) with concomitantly reduced activation of c-Jun N-terminal kinase (JNK) in the livers of WD-fed mice administered with GBCK25. Also, decreased cellular damage and inflammation were observed in alpha mouse liver 12 (AML12) cells and RAW264.7 cells, respectively. Conclusion: Administration of GBCK25 ameliorates NASH severity through the modulation of CYP2E1 and its associated JNK-mediated cellular damage. GBCK25 could be a potentially effective prophylactic strategy to prevent metabolic diseases including NASH.
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Choi, Naeun,Kim, Jong Won,Jeong, Hyeneui,Shin, Dong Gue,Seo, Jeong Hun,Kim, Jong Hoon,Lim, Chae Woong,Han, Kang Min,Kim, Bumseok The Korean Society of Ginseng 2019 Journal of Ginseng Research Vol.43 No.2
Background: Nonalcoholic steatohepatitis (NASH) is one of the chronic inflammatory liver diseases and a leading cause of advanced liver fibrosis, cirrhosis, and hepatocellular carcinoma. The main purpose of this study was to clarify the effects of GBCK25 fermented by Saccharomyces servazzii GB-07 and pectinase, on NASH severity in mice. Methods: Six-wk-old male mice were fed either a normal diet (ND) or a Western diet (WD) for 12 wks to induce NASH. Each group was orally administered with vehicle or GBCK25 once daily at a dose of 10 mg/kg, 20 mg/kg, 100 mg/kg, 200 mg/kg, or 400 mg/kg during that time. The effects of GBCK25 on cellular damage and inflammation were determined by in vitro experiments. Results: Histopathologic analysis and hepatic/serum biochemical levels revealed that WD-fed mice showed severe steatosis and liver injury compared to ND-fed mice. Such lesions were significantly decreased in the livers of WD-fed mice with GBCK25 administration. Consistently, mRNA expression levels of NASH-related inflammatory-, fibrogenic-, and lipid metabolism-related genes were decreased in the livers of WD-fed mice administered with GBCK25 compared to WD-fed mice. Western blot analysis revealed decreased protein levels of cytochrome P450 2E1 (CYP2E1) with concomitantly reduced activation of c-Jun N-terminal kinase (JNK) in the livers of WD-fed mice administered with GBCK25. Also, decreased cellular damage and inflammation were observed in alpha mouse liver 12 (AML12) cells and RAW264.7 cells, respectively. Conclusion: Administration of GBCK25 ameliorates NASH severity through the modulation of CYP2E1 and its associated JNK-mediated cellular damage. GBCK25 could be a potentially effective prophylactic strategy to prevent metabolic diseases including NASH.
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Kim, Jong-Won,Roh, Yoon-Seok,Jeong, Hyeneui,Yi, Ho-Keun,Lee, Min-Ho,Lim, Chae-Woong,Kim, Bumseok Elsevier 2018 The American journal of pathology Vol.188 No.4
<P>Excessive alcohol consumption leads to chronic liver diseases. Macrophage-inducible C-type lectin (MincLe) is a C-type lectin receptor that recognizes spliceosome-associated protein 130 (SAP130) known as an endogenous ligand released from dying cells. The aim was to examine the role of Mincle-SAP130 in the pathogenesis of alcoholic liver disease. Alcohol-induced liver injury was induced in wild-type (WT) and Mincle knockout (KO) mice by using a chronic-binge ethanol-feeding model. Mincle KO mice showed significant lower hepatic steatosis, inflammation with neutrophil infiltration, and fibrosis compared with WT mice after alcohol feeding. In contrast, Mincle activation exacerbated alcohol-induced liver injury. Kupffer cells (KCs) are major sources of Mincle. IL-1 beta expression was significantly down regulated in Mincle KO mice compared with that in WT mice after alcohol consumption. Interestingly, expression and production of IL-1 beta were significantly decreased in SAP130-treated KCs isolated from leucine-rich-containing family pyrin domain containing-3-deficient mice compared with those in WT KCs. Such results were also observed in cells treated with SAP130 plus Syk inhibitor. Furthermore, infiltration of invariant natural killer T cells was decreased in livers of Mincle KO mice. Finally, inhibition of Syk signaling ameliorated alcohol-induced liver injury. Collectively, these results demonstrated that interaction between Mincle and SAP130 may promote the progression of alcoholic Liver disease by IL-1 beta production in KCs and consequently increase inflammatory immune cell infiltration.</P>
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