http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
Irisin Regulates the Functions of Hepatic Stellate Cells
Hanh Nguyen Dong,박소영,Cong Thuc Le,최대희,조은희 대한내분비학회 2020 Endocrinology and metabolism Vol.35 No.3
Background: Hepatic stellate cells (HSCs) are known to play a fundamental role in the progression of liver fibrosis. Once HSCs areactivated, they are involved in proliferation, migration, and contractility which are characteristics of liver fibrogenesis. Recent studies have shown that irisin, a myokine secreted during physical exercise, has a protective effect in various metabolic diseases, especially in renal fibrosis. However, whether irisin is involved in HSC activation and other processes associated with liver fibrosis hasnot yet been investigated. In this study, we reveal the role of irisin in HSC activation as well as in proliferation, migration, and contractile properties of HSCs in vitro. Methods: LX-2 cells, immortalized human HSCs, were treated with transforming growth factor beta 1 (TGF-β1), a core regulator ofHSC fibrosis, with or without irisin, and markers of the aforementioned processes were analyzed. Further, an inflammatory responsewas stimulated with TGF-β1 and lipopolysaccharide (LPS) in combination with irisin and the expression of cytokines was measured. Results: Recombinant irisin significantly suppressed the expression of TGF-β1-stimulated fibrosis markers including alpha-smoothmuscle actin and collagen type 1 alpha 1 and prevented the TGF-β1-induced proliferation, migration, and contractility of LX-2 cells. Additionally, irisin ameliorated the production of interleukin-6 (IL-6) and IL-1β induced by TGF-β1 and LPS treatments. Conclusion: These findings suggested that irisin potently improved the progression of hepatic fibrosis by regulating HSC activation,proliferation, migration, contractility, and HSC-mediated production of inflammatory cytokine.
Nguyen, Tiep Tien,Pham, Tung Thanh,Nguyen, Hanh Thuy,Nepal, Mahesh Raj,Phung, Cao Dai,You, Zhiwei,Katila, Nikita,Pun, Nirmala Tillija,Jeong, Tae Cheon,Choi, Dong-Young,Park, Pil-Hoon,Yong, Chul Soon,K Elsevier 2019 Biomaterials Vol.221 No.-
<P><B>Abstract</B></P> <P>Host immune response remains an obstacle in cell-replacement therapy for treating type I diabetes. Long-term systemic immunosuppression results in suboptimal efficacy and adverse reactions. Thus, “cell-particle hybrids” of pancreatic islets and tissue-adhesive, polydopamine-coated, FK506-loaded biodegradable microspheres (PD-FK506-MS) were developed to locally modulate the immune response at the transplantation site. Coating of FK506-MS with PD enabled the rapid formation of stable cell-particle hybrids without significant changes in islet viability and functionality. Extremely low quantities of FK506 (approximately 600 ng per recipient) sustainably released from cell-particle hybrids effectively prolonged survival of xenogeneic islet graft. Interestingly, FK506 exhibited extended bioavailability in the grafts but was undetectable in systemic circulation and other tissues. Moreover, mRNA expression of inflammatory cytokines was significantly inhibited in the PD-FK506-MS-containing grafts but not in lymphoid organs. This study presents a promising platform that facilitates the translation of local immunomodulation towards an effective strategy with improved safety profiles for treating type I diabetes.</P>
Succinate Induces Liver Damage and Hepatic Fibrosis in a Mouse Model
레콩특,Nguyen, Giang,Dong, Hanh Nguyen,박소영,조윤경,최대희,박원선,이유진,이자영,조은희 계명대학교 의과대학 2022 계명의대학술지 Vol.41 No.2
Hepatic stellate cells (HSCs) play a key role in liver fibrosis. Succinate and succinate receptor (GPR91) signaling pathway are involved in the activation, proliferation, and migration of HSCs. We investigated whether succinate may induce hepatic fibrosis. The mice were randomly divided into 2 groups —the control group (chow diet-fed mice, n = 26) and sodium succinate group (2% sodium succinate + chow diet, n = 38). Each diet was provided for 16 weeks. Mice administered an oral diet of 2% sodium succinate for sixteen weeks lost body weight and had increased serum alanine transaminase and hepatic triglyceride contents compared to those in the control mice. Moreover, mice fed with sodium succinate showed increased expression of the alpha smooth muscle actin protein and gene in the liver at 8 weeks of feeding and increased fibrosis in their histology at 16 weeks of feeding. However, the expression of the GPR91 protein and mRNA increased at 4 weeks of feeding, but decreased at 8 and 16 weeks of feeding. These results suggest that an oral succinate diet could induce liver damage and liver fibrosis in mice and that GPR91 signaling might be an early marker or sensor of hepatic fibrosis development.
Phloretin Ameliorates Succinate-Induced Liver Fibrosis by Regulating Hepatic Stellate Cells
Cong Thuc Le,Giang Nguyen,박소영,Hanh Nguyen Dong,조윤경,이재호,임승순,최대호,조은희 대한내분비학회 2023 Endocrinology and metabolism Vol.38 No.4
Background: Hepatic stellate cells (HSCs) are the major cells which play a pivotal role in liver fibrosis. During injury, extracellular stimulators can induce HSCs transdifferentiated into active form. Phloretin showed its ability to protect the liver from injury, so in this research we would like to investigate the effect of phloretin on succinate-induced HSCs activation in vitro and liver fibrosis in vivo study. Methods: In in vitro, succinate was used to induce HSCs activation, and then the effect of phloretin on activated HSCs was examined. In in vivo, succinate was used to generated liver fibrosis in mouse and phloretin co-treated to check its protection on the liver. Results: Phloretin can reduce the increase of fibrogenic markers and inhibits the proliferation, migration, and contraction caused by succinate in in vitro experiments. Moreover, an upregulation of proteins associated with aerobic glycolysis occurred during the activation of HSCs, which was attenuated by phloretin treatment. In in vivo experiments, intraperitoneal injection of phloretin decreased expression of fibrotic and glycolytic markers in the livers of mice with sodium succinate diet-induced liver fibrosis. These results suggest that aerobic glycolysis plays critical role in activation of HSCs and succinate can induce liver fibrosis in mice, whereas phloretin has therapeutic potential for treating hepatic fibrosis. Conclusion: Intraperitoneal injection of phloretin attenuated succinate-induced hepatic fibrosis and alleviates the succinate-induced HSCs activation.
Pham, Tung Thanh,Nguyen, Hanh Thuy,Phung, Cao Dai,Pathak, Shiva,Regmi, Shobha,Ha, Dong-Ho,Kim, Jong Oh,Yong, Chul Soon,Kim, Sang Kyoon,Choi, Ji-Eun,Yook, Simmyung,Park, Jun-Beom,Jeong, Jee-Heon Elsevier 2019 Journal of industrial and engineering chemistry Vol.76 No.-
<P><B>Abstract</B></P> <P>Selective delivery of anti-cancer drugs to bone tumors remains an on-going developmental issue due to problems of drug availability and the physiological nature of bone. This study was undertaken to enhance accumulation of doxorubicin (DOX) in bone metastasis microenvironments using alendronate-functionalized graphene oxide nanosheets (NGO-ALs). In vivo biodistribution study showed NGO-ALs were retained for longer and at higher concentrations in bone tumor areas than non-functionalized NGOs. Our findings suggest that NGO-ALs could be used as a promising carrier to enhance antitumor effects and diminish the off-target effects of DOX for the treatment of bone metastasis.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
( Seung Hwan Kim ),( Thi Dieu Hanh Nguyen ),( Joo Hee Lee ),( Myoung Ki Hong ),( Tan Viet Pham ),( Yeh Jin Ahn ),( Byoung Moo Lee ),( Ye Sun Han ),( Dong Eun Kim ),( Jeong Gu Kim ),( Lin Woo Kang ) 한국미생물 · 생명공학회 2013 Journal of microbiology and biotechnology Vol.23 No.1
Xo2276 is a putative transcription activator-like effector (TALE) in Xanthomonas oryzae pv. oryzae (Xoo). Xo2276 was expressed with a TAP-tag at the C-terminus in Xoo cells to enable quantitative analysis of protein expression and secretion. Nearly all TAP-tagged Xo2276 existed in an insoluble form; addition of rice leaf extracts from a Xoosusceptible rice cultivar, Milyang23, significantly stimulated secretion of TAP-tagged Xo2276 into the medium. In a T3SS-defective Xoo mutant strain, secretion of TAPtagged Xo2276 was blocked. Xo2276 is a Xoo ortholog of Xanthomonas campestris pv. vesicatoria (Xcv) AvrBs3 and contains a conserved DNA-binding domain (DBD), which includes 19.5 tandem repeats of 34 amino acids. Xo2276- DBD was expressed in E. coli and purified. Direct in vitro recognition of Xo2276-DBD on a putative target DNA sequence was confirmed using an electrophoretic mobility shift assay. This is the first study measuring the homologous expression and secretion of Xo2276 in vitro using rice leaf extract and its direct in vitro binding to the specific target DNA sequence.