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Pluronic L-81 ameliorates diabetic symptoms in db/db mice through transcriptional regulation of microsomal triglyceride transfer protein

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World Journal of Gastroenterology 2009年第24期15卷 2987-2994页

作者： Wo-Shing Au Li-Wei Lu Sidney Tam otis king hung ko Billy KC Chow Ming-Liang He Samuel S Ng Chung-Man Yeung Ching-Chiu Liu Hsiang-Fu Kung Marie C Lin Institute of Molecular Technology for Drug Discovery and Synthesis Department of Chemistry The University of Hong Kong Hong Kong China Department of Pathology The University of Hong Kong Hong Kong China Division of Clinical Biochemistry Queen Mary Hospital Hong Kong China School of Biological Sciences The University of Hong Kong China Stanley Ho Center for Emerging Infectious Diseases The Chinese University of Hong Kong Shatin Hong Kong China

AIM: To test whether oral L-81 treatment could im-prove the condition of mice with diabetes and to investigate how L-81 regulates microsomal triglyceride transfer protein (MTP) activity in the liver. METHODS: Genetically diabetic (db/db) mice were fed on chow supplemented with or without L-81 for 4 wk. The body weight, plasma glucose level, plasma lipid profile, and adipocyte volume of the db/db mice were assessed after treatment. Toxicity of L-81 was also evaluated. To understand the molecular mecha-nism, HepG2 cells were treated with L-81 and the effects on apolipoprotein B (apoB) secretion and mRNA level of the MTP gene were ***: Treatment of db/db mice with L-81 sig-nificantly reduced and nearly normalized their body weight, hyperphagia and polydipsia. L-81 also markedly decreased the fasting plasma glucose level, improved glucose tolerance, and attenuated the elevated levels of plasma cholesterol and triglyceride. At the effective dosage, little toxicity was observed. Treatment of HepG2 cells with L-81 not only inhibited apoB secretion, but also signif icantly decreased the mRNA level of the MTP gene. Similar to the action of insulin, L-81 exerted its effect on the MTP promoter. CONCLUSION: L-81 represents a promising candidate in the development of a selective insulin-mimetic mol-ecule and an anti-diabetic agent.

关键词： Pluronic L-81 db/db mice Animal models diabetes Microsomal triglyceride protein

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A critical role of IL-17 in modulating the B-cell response during H5N1 influenza virus infection

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Cellular & Molecular Immunology 2011年第6期8卷 462-468页

作者： Xiaohui Wang Chris CS Chan Min Yang Jun Deng Vincent KM Poon Virtual HC Leung king-hung ko Jie Zhou Kwok Yung Yuen Bo-Jian Zheng Liwei Lu Department of Pathology The University of Hong KongHong KongChina Department of Microbiology The University of Hong KongHong KongChina Center of Infection and Immunology The University of Hong KongHong KongChina

Interleukin-17(IL-17),a member of the IL-17 cytokine family,plays a crucial role in mediating the immune response against extracellular bacteria and fungi in the *** there is increasing evidence that IL-17 is involved in protective immunity against H1 and H3 influenza virus infections,little is known about the role of IL-17 in the highly pathogenic H5N1 influenza virus *** this study,we show that H5N1-infected IL-17 knockout(ko)mice exhibit markedly increased weight loss,more pronounced lung immunopathology and significantly reduced survival rates as compared with infected wild-type ***,the frequency of B cells in the lung were substantially decreased in IL-17 ko mice after virus infection,which correlated with reduced CXCR5 expression in B cells and decreased CXCL13 production in the lung tissue of IL-17 ko *** with this observation,B cells from IL-17 ko mice exhibited a significant reduction in chemokine-mediated migration in *** together,these findings demonstrate a critical role for IL-17 in mediating the recruitment of B cells to the site of pulmonary influenza virus infection in mice.

关键词： B cell H5N1 influenza virus IL-17 lung infection

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Leptin Signaling Protects NK Cells from Apoptosis During Development in Mouse Bone Marrow

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Cellular & Molecular Immunology 2009年第5期6卷 353-360页

作者： Cherry Kam Chun Lo Queenie Lai Kwan Lam Min Yang king-hung ko Lingyun Sun Rui Ma Shengjun Wang Huaxi Xu Sidney Tam Chang-You Wu Bo-Jiang Zheng Liwei Lu Departments of Pathology and Microbiology Center of Infection andImmunology The University of Hong Kong Hong Kong China Department of Rheumatology Drum Tower Hospital Nanjing UniversityMedical School Nanjing China Department of Immunology School of Medical Science and LaboratoryMedicine Jiangsu University. Zhenjiang China epartment of Pathology Queen Mary Hospital Hong Kong China Department of Immunology Sun Yat-Sen University Guangzhou China These authors contributed equally to this work Department of Pathology and Center of Infection and Immunology The University of Hong Kong Pokfulam Road Hong Kong China

Increasing evidence indicates a role of leptin in immune response, but it remains largely unclear whether leptin signaling is involved in regulating NK cell development in the bone marrow （BM）. In this study, we have characterized NK cell differentiation and maturation in the BM of leptin-receptor deficient db/db mice at a prediabetic stage. Although the BM cellularity was similar to the control value, the total number of NK cells was severely reduced in mutant mice. Flow cytometric analysis of db/db BM cells revealed significantly decreased frequencies of developing NK cells at various stages of differentiation. BM db/db NK cells displayed markedly increased apoptosis but maintained normal cell cycling status and proliferative capacity. Moreover, recombinant leptin could significantly enhance the survival of NK cells from wild-type mice in cultures. Further examination on NK cell functional activity showed that db/db NK cells exhibited normal intrinsic cytotoxicity with significantly increased IL-10 production. Taken together, our findings suggest that leptin signaling regulates NK cell development via enhancing the survival of immature NK cells in mouse BM.

关键词： NK cell bone marrow lymphocyte development

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