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Liuweiwuling tablets attenuate acetaminophen-induced acute liver injury and promote liver regeneration in mice

World Journal of Gastroenterology 2015年第26期21卷 8089-8095页

作者： yan-chang lei Wen Li Pan Luo Department of Infectious Diseases Zhejiang Hospital Infectious Diseases Hospital of Nanchang University

AIM: To explore the mechanism of protection against acetaminophen-induced acute liver injury by Liuweiwuling ***: Intraperitoneal injections of acetaminophen(250 mg/kg) were used to induce acute liver injury in male C57BL/6 mice.A total of 24 healthy mice were randomly assigned to two groups: an acute liver injury group(control group) and a Liuweiwuling tablet *** were given Liuweiwuling tablets or a vehicle(PBS) orally prior to the administration of *** alanine aminotransferase(ALT) and aspartate aminotransaminase(AST) levels were measured at different time points within one week,and pathological examinations of liver tissues were performed 36 h after induction of acute liver *** inflammatory cytokines,such as high mobility group box protein B1(HMGB1),tumor necrosis factor(TNF)-α and interleukin IL-1b,were detected using an ELISA method according to the manufacturer's *** morphological changes at 36 h were assessed by hematoxylin and eosin *** of proliferating cell nuclear antigen(PCNA) in liver tissue was determined by Western blot *** m RNA levels of hepatocyte proliferation markers(PCNA,Cyclin D1 and p21) were detected by real-time quantitative reverse transcription-polymerase chain ***: The levels of ALT/AST in the Liuweiwuling tablet group were decreased significantly at 6,12 and 24 h compared to that of the control group(654.38 ± 120.87 vs 1566.17 ± 421.64,1154.18 ± 477.72 vs 4654.84 ± 913.71 and 935.13 ± 252.34 vs 4553.75 ± 727.37,P < 0.01).Serum HMGB1 levels at 6 and 12 h for the Liuweiwuling tablet group were significantly lower than those of the control group(23.49 ± 3.89 vs58.6 ± 3.65,61.62 ± 13.07 vs 27.32 ± 5.97,P < 0.01).Furthermore,serum TNF-α and IL-1b levels at 12 h in the Liuweiwuling tablet group were also significantly lower than those of the control group(299.35 ± 50.61 vs 439.03 ± 63.59,57.42 ± 12.98 vs 160.07 ± 49.87,P < 0.01).Centrilobular necr

关键词： Acute liver injury Acetaminophen Liuweiwulingtablets Inflammatory cytokine Liver regeneration

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Sphingosine kinase 1 dependent protein kinase C-δ activation plays an important role in acute liver failure in mice

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World Journal of Gastroenterology 2015年第48期21卷 13438-13446页

作者： yan-chang lei Ling-Ling yang Wen Li Pan Luo Department of Infectious Diseases Zhejiang Hospital Infectious Disease Hospital of Nanchang University

AIM: To investigate the role of protein kinase C(PKC)-δ activation in the pathogenesis of acute liver failure(ALF) in a well-characterized mouse model of D-galactosamine(D-Gal N)/lipopolysaccharide(LPS)-induced ***: BALB/c mice were randomly assigned to five groups, and ALF was induced in mice by intraperitoneal injection of D-Ga IN(600 mg/kg) and LPS(10 μg/kg). Kaplan-Meier method was used for survival analysis. Serum alanine aminotransferase(ALT) and aspartate aminotransferase(AST) levels at different time points within one week were determined using a multiparameteric analyzer. Serum levels of high-mobility group box 1(HMGB1), tumor necrosis factor(TNF)-α, interleukin(IL)-1β, IL-6, and IL-10 as well as nuclear factor(NF)-κB activity were determined by enzyme-linked immunosorbent assay. Hepatic morphological changes at 36 h after ALF induction were assessed by hematoxylin and eosin staining. Expression of PKC-δ in liver tissue and peripheral blood mononuclear cells(PBMCs) was analyzed by Western ***: The expression and activation of PKC-δ were up-regulated in liver tissue and PBMCs of mice with D-Gal N/LPS-induced ALF. Inhibition of PKC-δ activation with rottlerin significantly increased the survival rates and decreased serum ALT/AST levels at 6, 12 and 24 h compared with the control group(P < 0.001). Rottlerin treatment also significantly decreased serum levels of HMGB1 at 6, 12, and 24 h, TNF-α, IL-6 and IL-1 β at 12 h compared with the control group(P < 0.01). The inflammatory cell infiltration and necrosis in liver tissue were also decreased in the rottlerin treatment group. Furthermore, sphingosine kinase 1(Sph K1) dependent PKC-δ activation played an important role in promoting NF-κB activation and inflammatory cytokine production in ***: Sph K1 dependent PKC-δ activation plays an important role in promoting NF-κB activation and inflammatory response in ALF, and inhibition of PKC-δ activation might be a potential therapeutic strat

关键词： Acute liver failure Protein kinase C-δ Sphingosine kinase 1 Nuclear factor-κB

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Bone morphogenetic protein 4 induces cholinergic differentiation of brain-derived neural stem cells in vivo and in vitro

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Neural Regeneration Research 2010年第21期5卷 1611-1616页

作者： yan chang Jingkun Pan lei Tian Shuilong Guo Yun Luo Xin Cui Yilong Xue Laboratory of Cell Biology Institute of Geriatrics General Hospital of Chinese PLA Beijing 100853 China

In vitro studies have demonstrated that many factors of bone morphogenetic proteins （BMPs） induce cholinergic differentiation of neural stem cells. However, BMP retains the potential to induce increased numbers of cholinergic neurons in central nervous system regions that are rich in cholinergic cells, which is an important determinant of BMP. Therefore, BMP-4 was added to neural stem cell culture medium or the adult rat hippocampal dentate gyrus. Results demonstrated that BMP-4 induced cholinergic differentiation of neural stem cells in vitro and increased the number of cholinergic neurons in the adult rat hippocampal dentate gyrus.

关键词： bone morphogenetic protein neural stem cell induced differentiation cholinergic neuron neural regeneration

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Inhibition of sphingosine kinase 1 ameliorates acute liver failure by reducing high-mobility group box 1 cytoplasmic translocation in liver cells

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World Journal of Gastroenterology 2015年第46期21卷 13055-13063页

作者： yan-chang lei Ling-Ling yang Wen Li Pan Luo Pei-Fen Zheng Department of Infectious Diseases Zhejiang Hospital Infectious Disease Hospital of Nanchang University Department of Gastroenterology Zhejiang Hospital

AIM: To determine the therapeutic potential of sphingosine kinase 1(Sphk1) inhibition and its underlying mechanism in a well-characterized mouse model of D-galactosamine(D-Gal N)/lipopolysaccharide(LPS)-induced acute liver failure(ALF).METHODS: Balb/c mice were randomly assigned to different groups,with ALF induced by intraperitoneal injection of D-Ga IN(600 mg/kg) and LPS(10 μg/kg). The Kaplan-Meier method was used for survival analysis. Serum alanine aminotransferase(ALT) and aspartate aminotransferase(AST) levels at different time points within one week were determined using a multi-parametric analyzer. Serum high-mobility group box 1(HMGB1),tumor necrosis factor-α(TNF-α),interleukin(IL)-1β,IL-6,IL-10,and sphingosine-1-phosphate were detected by enzyme-linked immunosorbent assay. Hepatic morphological changes at 36 h after acute liver injury induction were assessed by hematoxylin and eosin staining. HMGB1 expression in hepatocytes and cytoplasmic translocation were detected by immunohistochemistry. Expression of Sphk1 in liver tissue and peripheral blood mononuclear cells(PBMCs) was analyzed by Western ***: The expression of Sphk1 in liver tissue and PBMCs was upregulated in Gal N/LPS-induced ALF. Upregulated Sphk1 expression in liver tissue was mainly caused by Kupffer cells,the resident macrophages of the liver. The survival rates of mice in the N,Ndimethylsphingosine(DMS,a specific inhibitor of Sph K1) treatment group were significantly higher than that of the control group(P < 0.001). DMS treatment significantly decreased the levels of serum ALT and AST at 6,12,and 24 h compared with that of the control group(P < 0.01 for all). Serum HMGB1 levels at 6,12,and 24 h,as well as serum TNF-α,IL-6,and IL-1β levels at 12 h,were significantly lower in the DMS treatment group than in the control group(P < 0.01 for all). Furthermore,hepatic inflammation,necrosis,and HMGB1 cytoplasm translocation in liver cells were significantly decreased in the DMS treatment g

关键词： Acute liver failure Sphingosine kinase 1 High-mobi

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C5a/C5a R pathway is essential for up-regulating Sph K1 expression through p38-MAPK activation in acute liver failure

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World Journal of Gastroenterology 2016年第46期22卷 10148-10157页

作者： yan-chang lei Chun-lei Lu Ling Chen Ke Ge Ling-Ling yang Wen Li Yuan-Hua Wu Department of Infectious Diseases Zhejiang Hospital Hangzhou 310013 Zhejiang Province China Infectious Diseases Hospital of Nanchang University Nanchang 3300036 Jiangxi Province China The First People’s Hospital of Pinghu Pinghu 314200 Zhejiang Province China

AIM To investigate the role of the complement 5a(C5a)/C5 a receptor(C5a R) pathway in the pathogenesis of acute liver failure(ALF) in a mouse *** BALB/c mice were randomly assigned to different groups, and intraperitoneal injections of lipopolysaccharide(LPS)/D-galactosamine(D-Gal N)(600 mg/kg and 10 μg/kg) were used to induce ALF. The KaplanMeier method was used for survival analysis. Serum alanine aminotransferase(ALT) levels, at different time points within a 1-wk period, were detected with a biochemistry analyzer. Pathological examination of liver tissue was performed 36 h after ALF induction. Serum complement 5(C5), C5 a, tumor necrosis factor-α(TNF-α), interleukin(IL)-1β, IL-6, high-mobility group protein B1(HMGB1) and sphingosine-1-phosphatelevels were detected by enzyme-linked immunosorbant assay. Hepatic morphological changes at 36 h after ALF induction were assessed by hematoxylin and eosin staining. Expression of C5 a R, sphingosine kinase 1(Sph K1), p38-MAPK and p-p38-MAPK in liver tissue, peripheral blood mononuclear cells(PBMCs) and peritoneal exudative macrophages(PEMs) of mice or RAW 264.7 cells was analyzed by western blotting. C5 a R m RNA levels were detected by quantitative real-time *** Activation of C5 and up-regulation of C5 a R were observed in liver tissue and PBMCs of mice with ALF. Blockade of C5 a R with a C5 a R antagonist(C5a Ra C5 a Ra) significantly reduced the levels of serum ALT, inflammatory cytokines(TNF-α, IL-1β and IL-6) and HMGB1, as well as the liver tissue damage, but increased the survival rates(P < 0.01 for all). Blockade of C5 a R decreased Sph K1 expression in both liver tissue and PBMCs significantly at 0.5 h after ALF induction. C5 a Ra pretreatment significantly downregulated the phosphorylation of p38-MAPK in liver tissues of ALF mice and C5 a stimulated PEMs or RAW 264.7 cells. Moreover, inhibition of p38-MAPK activity with SB203580 reduced Sph K1 protein production significantly in PEMs after C5 a

关键词： Acute liver failure C5a/C5a R p38-MAPK Sphingosine kinase 1

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Effect of Hepatitis C Virus Core Protein on Interferon-Induced Antiviral Genes Expression and Its Mechanisms

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中国病毒学 2007年第5期22卷 374-379页

作者： yan-zi chang yan-chang lei Wen WU Shan-shan CHEN Han-ju HUANG Dong-liang yanG Meng-ji LU Department of Pathogen Biology Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China Division of Clinical Immunology Tongji Hospital Huazhong University of Science and Technology Wuhan 430030 China.

Emerging data indicated that HCV subverts the antiviral activity of interferon(IFN);however,whether HCV core protein contributes to the process remains *** the present study,we examined the effect of HCV core protein on interferon-induced antiviral gene expression and whether the effect is involved in the activation and negative regulation of the Jak/STAT signaling *** results showed that,following treatment with IFN-α,the transcription of PKR,MxA and 2'-5'OAS were down-regulated in HepG2 cells expressing the core *** the presence of HCV core protein,ISRE-dependent luciferase activity also *** study indicated that the core protein could inhibit the tyrosine phosphorylation of STAT1,whereas the level of STAT1 expression was ***,SOCS3,the negative regulator of the Jak/STAT pathway,was induced by HCV core *** results suggests that HCV core protein may interfere with the expression of some interferon-induced antiviral genes by inhibiting STAT1 phosphorylation and induction of SOCS3.

关键词：丙型肝炎病毒核心蛋白质 α-干扰素抗病毒基因表达作用机理

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Inhibition of hepatitis B virus replication by APOBEC3G in vitro and in vivo

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World Journal of Gastroenterology 2006年第28期12卷 4492-4497页

作者： yan-chang lei You-Hua Hao Zheng-Mao Zhang Yong-Jun Tian Bao-Ju Wang yan yang Xi-Ping Zhao Meng-Ji Lu Fei-Li Gong Dong-Liang yang Division of Clinical Immunology Department of Infectious Diseases Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology. Wuhan 430030. Hubei Province. China Center of Experimental Medicine Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 Hubei Province China Department of Microbiology Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 Hubei Province China Department of Immunology Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 Hubei Province China 不详

AIM： To investigate the effect of APOBEC3G mediated antiviral activity against hepatitis B virus （HBV） in cell cultures and replication competent HBV vector-based mouse model. METHODS： The mammalian hepatoma cells Huh7 and HepG2 were cotransfected with various amounts of CMV-driven expression vector encoding APOBEC3G and replication competent 1.3 fold over-length HBV. Levels of HBsAg and HBeAg in the media of the transfected cells were determined by ELISA. The expression of HBcAg in transfected cells was detected by western blot. HBV DNA and RNA from intracellular core particles were examined by Northern and Southern blot analyses. To assess activity of the APOBEC3G in vivo, an HBV vector-based model was used in which APOBEC3G and the HBV vector were co-delivered via high-volume tail vein injection. Levels of HBsAg and HBV DNA in the sera of mice as well as HBV core-associated RNA in the liver of mice were determined by ELISA and quantitative PCR analysis respectively. RESULTS： There was a dose dependent decrease in the levels of intracellular core-associated HBV DNA and extracellular production of HBsAg and HBeAg. The levels of intracellular core-associated viral RNA also decreased, but the expression of HBcAg in transfected cells showed almost no change. Consistent with in vitro results, levels of HBsAg in the sera of mice were dramatically decreased. More than 1.5 log10 decrease in levels of serum HBV DNA and liver HBV RNA were observed in the APOBEC3G-treated groups compared with the control ***： These findings indicate that APOBEC3G could suppress HBV replication and antigen expression both in vivo and in vitro, promising an advance in treatment of HBV infection.

关键词： APOBEC3G Hepatitis B virus Antiviral therapy

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N-terminal and C-terminal cytosine deaminase domain of APOBEC3G inhibit hepatitis B virus replication

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World Journal of Gastroenterology 2006年第46期12卷 7488-7496页

作者： yan-chang lei Yong-Jun Tian Hong-Hui Ding Bao-Ju Wang yan yang You-Hua Hao Xi-Ping Zhao Meng-Ji Lu Fei-Li Gong Dong-Liang yang Division of Clinical Immunology Department of Infectious Disease Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 Hubei Province China Center of Experimental Medicine Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 Hubei Province China Department of Microbiology Tongji Medical College Huazhong University of Science and Technology Wuhan430030 Hubei Province China Institute of Virology Medical School of Duisburg-Essen University Essen Germany Department of Immunology Tongji Medical College Huazhong University of Science and Technology Wuhan430030 Hubei Province China

AIM: To investigate the effect of human apolipoprotein B mRNA-editing enzyme catalytic-polypeptide 3G (APOBEC3G) and its N-terminal or C-terminal cytosine deaminase domain-mediated antiviral activity against hepatitis B virus (HBV) in vitro and in vivo. METHODS: The mammalian hepatoma cells HepG2 and HuH7 were cotransfected with APOBEC3G and its N-terminal or C-terminal cytosine deaminase domain expression vector and 1.3-fold-overlength HBV DNA as well as the linear monomeric HBV of genotype B and C. For in vivo study, an HBV vector-based mouse model was used in which APOBEC3G and its N-terminal or C-terminal cytosine deaminase domain expression vectors were co-delivered with 1.3-fold-overlength HBV DNA via high-volume tail vein injection. Levels of hepatitis B virus surface antigen (HBsAg) and hepatitis B virus e antigen (HBeAg) in the media of the transfected cells and in the sera of mice were determined by *** expression of hepatitis B virus core antigen (HBcAg) in the transfected cells was determined by Western blot analysis. Core-associated HBV DNA was examined by Southern blot analysis. Levels of HBV DNA in the sera of mice as well as HBV core-associated RNA in the liver of mice were determined by quantitative PCR and quantitative RT-PCR analysis, respectively. RESULTS: Human APOBEC3G exerted an anti-HBV activity in a dose-dependent manner in HepG2 cells, and comparable suppressive effects were observed on genotype B and C as that of genotype A. Interestingly, the N-terminal or C-terminal cytosine deaminase domain alone could also inhibit HBV replication in HepG2 cells as well as Huh7 cells. Consistent with in vitro results, the levels of HBsAg in the sera of mice were dramatically decreased, with more than 50 times decrease in the levels of serum HBV DNA and core-associated RNA in the liver of mice treated with APOBEC3G and its N-terminal or C-terminal cytosine deaminase domain as compared to the controls. CONCLUSION: Our findings provide probably the f

关键词： Cytosine deaminase domain Apolipoprotein B mRNA-editing enzyme catalytic-polypeptide 3G Hepatitis B virus Antiviral therapy

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Induction of APOBEC3G in human hepatoma cells by interferon-α stimulation

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Journal of Microbiology and Immunology 2006年第3期4卷 222-230页

作者： yan chang lei YONG WEN HE CHUN XIA GUO Department of Infectious Disease Union Hospital Ton~i Medical College Huazhong University of Scienceand Technology Wuhan P. R. China.

To clarify the role of APOBEC3G （A3G） in cellular defense against hepatitis B virus （HBV）, the expression of A3G in normal human liver and the regulation of the A3G expression in hepatoma cell line （HuH-7） were investigated. Expression level of APOBEC3s mRNA in human liver was determined by RT-PCR. HuH-7 and HepG2 cells were treated with various concentrations of IFN-α（0 U/ml, 100 U/ml, 500 U/ml, 1000 U/ml）for 12 h. The mRNA levels were measured by a quantitative RT-PCR, the results were normalized relative to the specimens without IFN-α stimulation. Total protein of HuH-7 cells treated with various concentrations of IFN-α for 48 h was subjected to Western blot analysis. For reporter gene assay, HuH-7 cells were transfected with the reporter plasmids containing IRF- E sites and its mutants with different lengths. Then the cells were treated with or without 1200 U/ml IFN-α for additional 12 h （ 1000 U/ml） after 24 h of transfection, and the cell lysate was prepared and assayed for lueiferase activity. It was found that normal human liver expressed the rnR_NA of A3G. A3G mRNA expression in HuH-7 and HepG2 cells were up-regulated by IFN-α stimulation in a dose-depen- dent manner. Western blot analysis indicated that A3G protein expression was also enhanced by IFN-α stimulation. Sequence analysis showed the existence of putative sites of IFN regulatory factor element （IRF-E） in 5＇ region of A3G gene upstream the initiation eodon. IFN-α stimulation results in 6- to 8- fold increase in lueiferase activity in cells transfeeted with the plasmid containing IRF-E sites of the 5＇ upstream sequences, whereas luciferase activity did not change in cells transfected with the plasmid containing mutant IRF-E sites or without IRF-E sites. As a conclusion, A3G are expressed in normal human liver. A3G expression was up-regulated by IFN-α stimulation in hepatoma cells and could be involved in host defense mechanisms against HBV. IRF-E site in 5＇ region of APOBEC3G gene upstream the init

关键词： APOBEC3G IFN-α Hepatoma cell IRF-E

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Isolation, Cloning, and Identification of Expressed Sequence Tags from the Backfat Tissue in Duroc and Tongcheng Pigs by mRNA Differential Display

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Agricultural Sciences in China 2006年第2期5卷 141-145页

作者： REN Zhu-qing XIONG Yuan-zhu DENG chang-yan lei Ming-gang ZUO Bo LI Feng-e ZHENG Rong XU De-quan Key Laboratory of Swine Breeding and Genetics Ministry of Agriculture/Huazhong Agricultural University Wuhan 430070 P.R.China

mRNA differential display technique was performed to discuss the differential expression of genes in fat tissue between introduced European and Chinese indigenous pigs. Four anchor primers in combination with five arbitrary primers （20 sets in total） were used and nearly 300 bands were observed in polyacrylamide gel, among which 29 differential display bands were obtained. Twelve of 29 cDNA fragments were identified using reverse Northern dot blot, and subsequently cloned and sequenced. Eight of 12 cDNAs had no matches in GenBank and were submitted to GenBank, and the other 4 showed similarity to identified genes from GenBank. Three among 8 novel ESTs were selected to be further identified by semiquantitative RT-PCR. In our experiment, silver staining DDRT-PCR and DIG primer DNA labeling reverse Northern dot blot were used to avoid radioactive pollution. The result showed that the expressions of 5 among 8 novel ESTs were stronger in the backfat of Tongcheng pigs and the others were weaker than that in Duroc pigs. These novel ESTs were prepared for selecting genes related to adipose cells.

关键词： ESTs fat tissue reverse Northern dot blot semi-quantitative RT-PCR mRNA differential display

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