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왕시형,이찬빈,김지은,현정은,임민소,차혁진,오세훈,최영현,정영미 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
Tumor necrosis factor-inducible gene 6 protein (TSG-6) has recently been shown to protect the liver from acute damage. However, the mechanism underlying the effect of TSG-6 on the liver remains unclear. Autophagy is a catabolic process that targets cell components to lysosomes for degradation, and its functions are reported to be dysregulated in liver diseases. Here we investigate whether TSG-6 promotes liver regeneration by inducing autophagic clearance in damaged livers. Mice fed a methionine choline-deficient diet supplemented with 0.1% ethionine (MCDE) for 2 weeks were injected with TSG-6 (the M+TSG-6 group) or saline (the M+V group) and fed with MCDE for 2 additional weeks. Histomorphological evidence of injury and increased levels of liver enzymes were evident in MCDE-treated mice, whereas these symptoms were ameliorated in the M+TSG-6 group. Livers from this group contained less active caspase-3 and more Ki67-positive hepatocytic cells than the M+V group. The autophagy markers ATG3, ATG7, LC3-II, LAMP2A and RAB7 were elevated in the M+TSG-6 group compared with those in the M+V group. Immunostaining for LC3 and RAB7 and electron microscopy analysis showed the accumulation of autophagy structures in the M+TSG-6 group. TSG-6 also blocked both tunicamycin- and palmitate-induced apoptosis of hepatocytes and increased their viability by inducing autophagy formation in these cells. An autophagy inhibitor suppressed TSG-6-mediated autophagy in the injured hepatocytes and livers of MCDE-treated mice. These results therefore demonstrate that TSG-6 protects hepatocytes from damage by enhancing autophagy influx and contributes to liver regeneration, suggesting that TSG-6 has therapeutic potential for the treatment of liver diseases.
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왕시형(Sihyung Wang),정영미(Youngmi Jung) 한국생명과학회 2013 생명과학회지 Vol.23 No.5
방사선 치료는 가장 일반적으로 사용되고 있는 항암치료로, 암 환자의 수 증가와 동반하여 방사선 활용도는 더욱 증가하고 있다. 방사선치료에 대한 환자들의 심리적 거부감과 산화적 스트레스, 저산소증, DNA 손상을 포함하여, 치료 후 나타나는 간 섬유화는 방사선 치료의 가장 큰 문제점으로 대두되고 있다. 간암의 경우 대부분의 환자들이 섬유화를 동반하고 있어서, 방사선에 의해 암세포가 제거된다 하더라도, 기존에 남아있는 손상 부위에서의 섬유화와 방사선 조사에 의한 정상조직의 섬유화는 간경변 유발 확률을 높이고 있다. 간 섬유화는 여러 간질환에서 흔히 관찰되는 증상으로, 간 섬유화 진행 기작의 규명은 만성질환으로의 진행을 억제할 수 있는 치료책 개발로 연계될 수 있지만, 아직까지 명확히 규명되지 않음에 따라, 섬유화를 억제할 수 있는 효과적인 방법이 없는 실정이다. 최근 간 섬유화 생성 및 진행에 대한 헤지호그의 역할이 밝혀지면서, 간암 및 만성질환으로의 진행을 이해하기 위한 연구대상으로 대두되고 있다. 헤지호그는 손상된 간에서 발현되어 보수과정에 기여하게 된다. 헤지호그의 발현은 간 손상 정도에 비례하여 발현되어, 간 줄기세포 및 간 성상세포의 증식을 조절한다. 또한, TGF-β1와, EMT를 유도하고 근섬유화세포의 활성을 조절하여, 간 섬유화 진행에 중심적 역할을 한다. 방사선이 조사된 생쥐의 간에서도 헤지호그의 발현증가가 관찰되었고, 이에 따른 간 줄기세포의 증식 및 EMT 유도, 콜라겐의 축적이 관찰되었다. 또한, 방사선이 조사된 암컷 생쥐의 간에서 헤지호그의 차별적 증가는 줄기세포 및 섬유화 증대로 연결되었고, 이는 방사선 민감성에 대한 성별차이를 설명할 수 있는 생물학적 근거가 될 수 있다. 그러나, 방사선에 의해 유도된 간 섬유화에 대한 연구결과들이 헤지호그를 비롯하여, 표면적인 결과보고만 있을 뿐, 섬유화 진행에 대한 구체적 기작을 밝히지 못하고 있다. 여러 간 질환진행에서 규명된 헤지호그 작용에 대한 지식을 방사선에 의해 유도된 간 섬유화를 이해하기 위한 기초자료로 활용하고, 사람에서의 방사선 부작용과 유사한 동물모델의 정립 및 헤지호그 역할을 직접적으로 규명할 수 있는 추가적 연구을 통해서, 간 섬유화 형성 기작을 이해할 수 있는 연구결과가 기대된다. Radiotherapy is commonly used in treating many kinds of cancers which cannot be cured by other therapeutic strategies. However, radiotherapy also induces the damages on the normal tissues. Radiation-induced fibrosis is frequently observed in the patients undergoing radiotherapy, and becomes a major obstacle in the treatment of intrahepatic cancer. Hedgehog (Hh) that is an essential in the liver formation during embryogenesis is not detected in the healthy liver, but activated and modulates the repair process in damaged livers in adult. The expression of Hh increases with the degree of liver damage, regulating the proliferation of hepatic progenitors and hepatic stellate cells (HSC). In addition, Hh induces epithelial-to-mesencymal transition (EMT) and activation of myofibroblasts. In the irradiated livers, up-regulated expression of Hh signaling was associated with proliferation of progenitors, EMT induction, and increased fibrosis. Female-specific expression of Hh leaded to the expansion of progenitors and the accumulation of collagen in the irradiated livers of female mice, indicating that gender disparity in Hh expression may be related with radiation-susceptibility in female. Hence, Hh signaling becomes a novel object of studies for fibrogenesis induced by radiation. However, the absence of the established experimental animal models showing the similar physiopathology with human liver diseases and fibrosis-favorable microenvironment hamper the studies for the radiation-induced fibrosis, providing a few descriptive results. Therefore, further research on the association of Hh with radiation-induced fibrosis can identify the cell and tissue-specific effects of Hh and provides the basic knowledge for underlying mechanisms, contributing to developing therapies for preventing the radiation-induced fibrosis.
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Kombucha Tea Prevents Obese Mice from Developing Hepatic Steatosis and Liver Damage
현정은,이영재,왕시형,김진년,김지은,차재호,서영수,정영미 한국식품과학회 2016 Food Science and Biotechnology Vol.25 No.3
Nonalcoholic fatty liver disease (NAFLD) is associated with the increased accumulation of hepatocellular lipids. Although Kombucha tea (KT) has emerged as a substance protecting the liver from damage, the effects of KT in NAFLD remain unclear. Hence, we investigated whether KT influenced hepatic steatosis. Db/db mice were fed either control or methionine/choline-deficient (MCD) diets for 4 weeks. The MCD diet group was treated with KT or water for 3 weeks. KT treatment alleviated macrovesicular steatosis compared to the MCD-fed group. The levels of triglyceride, ALT, and AST also decreased in the KT+MCD-treated db/db mice. RNA expression in the MCD+KT group showed reduced triglyceride synthesis and uptake of fatty acids. Immunostaining and western blot assays for active caspase-3 demonstrated a lower level of apoptosis in the MCD+KT than in the MCD group. These results demonstrate that KT attenuated lipid accumulation and protected the liver from damage, promoting liver restoration in mice.
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Effect of Kombucha on gut-microbiota in mouse having non-alcoholic fatty liver disease
정영미,김인영,Mohamed Mannaa,김진년,왕시형,박인명,김지은,서영수 한국식품과학회 2019 Food Science and Biotechnology Vol.28 No.1
Non-alcoholic fatty liver disease (NAFLD) isone of the most common liver disorders. Possible linkshave been recently found between the gut-microbiota andthe host metabolism in development of NAFLD and obesity. Therefore, understanding the changes in intestinalmicrobiota during the progression of NAFLD, is important. In this study, the effect of Kombucha tea (KT), obtained bymicrobial fermentation of sugared black tea, was investigatedon gut-microbiota during the progression of NAFLD. The results indicated a decrease in Erysipelotrichia class bytreatment with KT in comparison to the methionine/choline-deficient (MCD)-fed db/db mice. Allobaculum,Turicibacter, and Clostridium genera, were only detectedin MCD-fed db/db mice and were decreased after treatmentwith KT, whereas Lactobacillus was more abundant inMCD ? KT-fed mice than in MCD only-fed mice andMucispirillum, was found only in the MCD ? KT-fedmice group. Our results demonstrated that the change ofintestinal microbiota was influenced by KT intake, contributingto combat NAFLD.
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