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Tao Wen

Publications and source records attributed to Tao Wen.

12 recordsLinked to original sources
PubMed2006

Protective effects of echinacoside on carbon tetrachloride-induced hepatotoxicity in rats.

The aim of this study was to investigate the possible protective effects of echinacoside, one of the phenylethanoids isolated from the stems of Cistanches salsa, a Chinese herbal medicine, on the free radical damage of liver caused by carbon tetrachloride in rats. Treatment of rats with carbon tetrachloride produced severe liver injury, as demonstrated by dramatic elevation of serum ALT, AST levels and typical histopathological changes including hepatocyte necrosis or apoptosis, haemorrhage, fatty degeneration, etc. In addition, carbon tetrachloride administration caused oxidative stress in rats, as evidenced by increased reactive oxygen species (ROS) production and MDA concentrations in the liver of rats, along with a remarkable reduction in hepatic SOD activity and GSH content. However, simultaneous treatment with echinacoside (50mg/kg, intraperitoneally) significantly attenuated carbon tetrachloride-induced hepatotoxicity. The results showed that serum ALT, AST levels and hepatic MDA content as well as ROS production were reduced dramatically, and hepatic SOD activity and GSH content were restored remarkably by echinacoside administration, as compared to the carbon tetrachloride-treated rats. Moreover, the histopathological damage of liver and the number of apoptotic hepatocytes were also significantly ameliorated by echinacoside treatment. It is therefore suggested that echinacoside can provide a definite protective effect against acute hepatic injury caused by CCl(4) in rats, which may mainly be associated with its antioxidative effect.

Alanine Transaminase↗
PubMed2006

[Protective effect of heme oxygenase-1 and its reaction product, carbon monoxide on acute liver injury induced by carbon tetrachloride in rats].

OBJECTIVE: To investigate the protective role of heme oxygenase-1 and its reaction product, carbon monoxide against acute liver injury induced by carbon tetrachloride in rats. METHODS: Thirty male Sprague-Dawley rats were randomly divided into six groups with five in each. The control group received a single dose of corn oil injection. Carbon tetrachloride was injected intraperitoneally (i.p) to establish acute liver injury models in rats. Hemin(50 micromol/kg) was administered i.p. 12 hours before CCl(4) treatment, with an aim to induce HO-1 protein expression in the liver of rats. Carbon monoxide was injected i.p. 12 hours prior to CCl(4) injection, resulting in about 8%-12% carboxyhemoglobin concentration in vivo. The expression of HO-1 in the liver of hemin-treated rats was determined by western blot method at different time points. At 24 h after carbon tetrachloride administration, all rats were sacrificed to collect blood samples for the examination of ALT, AST levels and to remove liver tissues for analysis of MDA concentration, SOD activity and caspase-3 activity as well as TNF-alpha contents. In addition, histopathological changes were investigated and hepatocyte apoptosis was detected by TUNEL method. RESULTS: The administration of carbon tetrachloride to rats caused a marked hepatic damage, characterized by significant elevation of serum ALT, AST levels(2 136.3+/-163.4 U, 1 422.7+/-221.7 U) and liver MDA content(5.28+/-0.93 micromol/g), caspase-3 activity (optical density value 4.69+/-1.02) and TNF-alpha level(256.3+/-27.3 ng/L) combined with a remarkable reduction in liver SOD activity (45.9+/-14.8 U/mg) as compared with the control rats. Histopathological observations revealed severe damage in the liver and prominent hepatocyte apoptosis took place in CCl(4) -treated rats. However, pretreatment with hemin could induce high expression of HO-1 protein and exert potent protective effects against liver injury, as demonstrated by a significant decrease in ALT, AST levels(287.1+/-24.3 U, 246.2+/- 21.7 U) and MDA concentration(3.27+/-1.34 micromol/g), reduction in caspase-3 activity(optical density value 2.49+/-1.47) and TNF-alpha level(132.6+/-19.5 ng/L), as compared with the CCl(4) -treated rats. Moreover, hepatocyte apoptosis and liver injury were both attenuated remarkably in the liver of rats pretreated with hemin. In contrast to hemin administration, single injection of exogenous CO produced the same protective effects, as indicated by the remarkable reduction of ALT, AST levels and caspase-3 activity and TNF-alpha levels. CONCLUSION: The above results suggest that HO-1/CO system has a potent protective effect on acute liver injury induced by carbon tetrachloride in rats. Induction of HO-1 expression and low concentration of CO can inhibit the progress of hepatic damage, which might be due to the alleviation of lipid peroxidation and reduction of caspase-3 activity or inhibition of TNF-alpha level.

Alanine Transaminase↗
PubMed2006

Dynamic changes of heme oxygenase-1 and carbon monoxide production in acute liver injury induced by carbon tetrachloride in rats.

Heme oxygenase-1, a stress-responsive enzyme that catabolizes hemes into carbon monoxide, biliverdin, and iron, has been shown to play a pivotal role in many physiological and pathological situations. Here we investigated changes in HO-1 enzyme activity and protein expression, and its end product carbon monoxide concentrations in the liver of rats after CCl(4) treatment. We found that CCl(4) administration not only induced severe liver damage in rats, as demonstrated by dramatic elevation of ALT, AST levels and severe histopathological changes, but also resulted in a prominent up-regulation of HO-1 enzyme activity. Western blot and immunohistochemical analysis confirmed that expression of HO-1 protein was also increased significantly in a time-dependent manner following CCl(4) treatment, and localized mainly in liver cells around the central vein. In addition, CO concentrations in the liver of CCl(4)-treated rats were elevated remarkably in the same time-dependent way as HO-1 induction in contrast to the control rats. These data indicated that HO-1/CO pathway was greatly up regulated in the liver of rats after CCl(4) treatment, which might play an important protective role in the pathophysiological mechanism underlying CCl(4)-induced hepatotoxicity. It therefore suggested that more relevant studies should be carried out in the future to clarify the detailed mechanisms.

Alanine Transaminase↗
PubMed2006

[Expression of Fas antigen and Fas ligand in acute liver injury induced by carbon tetrachloride in rat].

OBJECTIVE: To investigate the dynamics of expression of Fas antigen and Fas ligand (FasL) in a rat model of carbon tetrachloride-induced acute liver injury, and explore the role of apoptosis in liver injury. METHODS: Thirty-five healthy male Wistar rats were randomly divided into normal control group and experiment group, and the latter group was divided into six subgroups: 3, 9, 16, 24, 36 and 48 hours groups with 5 rats in each group. The liver injury was induced by carbon tetrachloride. Sections of liver tissue were stained with hematoxylin and eosin and observed under optical microscope. Fas antigen and FasL in rat liver were determined at different time points with immunohistochemical method. Hepatocytes apoptosis were observed with terminal deoxynucleotidyl-transferase mediated dUTP-biotin nick end labeling (TUNEL) method. Superoxide dismutase (SOD) activity and malondialdehyde (MDA) concentration in the liver tissues were analyzed at the same time point. Serum aspartate aminotransferase (ALT) and alanine aminotransferase (AST) levels were also determined. RESULTS: Fas antigen and FasL were expressed in the liver tissues of control rats. Following carbon tetrachloride challenge, severe liver injury took place in rats as revealed under microscope and a large amount of hepatocytes apoptosis was found. Hepatic Fas and FasL expression were both increased markedly from 3 to 48 hours after carbon tetrachloride challenge in experiment group. Liver MDA concentration and serum ALT and AST were elevated significantly, while SOD activity decreased remarkably in the experiment group compared with control group (P<0.05 or P<0.01). CONCLUSION: Expression of Fas/FasL is remarkably induced in acute liver injury and accords with the changes of hepatocytes apoptosis, which suggests that apoptosis mediated by Fas/FasL may play an important role in the pathogenesis of acute liver injury.

Animals↗
PubMed2005

Evaluation of OX40 ligand as a costimulator of human antiviral memory CD8 T cell responses: comparison with B7.1 and 4-1BBL.

CTL are important effectors of antiviral immunity. Designing adjuvants that can induce strong cytotoxic T cell responses in humans would greatly improve the effectiveness of an antiviral vaccination or therapeutic strategy. Recent evidence suggests that, in addition to its well-established role in costimulation of CD4 T cell responses, OX40L (CD134) can directly costimulate mouse CD8 T cells. In this study, we evaluated the role of OX40L in costimulation of human antiviral CD8 T cell responses and compared it with two other important costimulators, B7.1 (CD80) and 4-1BBL (CD137L). Delivery of OX40L to human monocytes using a recombinant replication-defective adenovirus led to greater expansion, up-regulation of perforin, enhanced cytolytic activity, and increased numbers of IFN-gamma- and TNF-alpha-producing antiviral memory CD8 T cells in cultures of total T cells. Synergistic or additive effects were observed when OX40L costimulation was combined with 4-1BBL (CD137L) or B7.1 (CD80) costimulation. In total T cell cultures, at low Ag dose, 4-1BBL provided the most potent costimulus for influenza-specific CD8 T cell expansion, followed by B7.1 (CD80) and then OX40L. For isolated CD8 T cells, 4-1BBL was also the most consistent costimulator, followed by B7.1. In contrast, OX40L showed efficacy in direct activation of memory CD8 T cells in only one of seven donors. Thus, OX40L costimulates human antiviral memory CD8 T cell responses largely through indirect effects and can enhance anti-influenza, anti-EBV, and anti-HIV responses, particularly in combination with 4-1BBL or B7.

4-1BB Ligand↗
PubMed2005

Enhancement of HIV-specific CD8 T cell responses by dual costimulation with CD80 and CD137L.

HIV-specific CD8 T cell responses are defective in chronic HIV infection. In this study, we report that costimulation with either CD137L (4-1BBL) or CD80 (B7.1) enhanced the Ag-specific expansion and acquisition of effector function by HIV-specific memory CD8 T cells. Ag-specific T cells from recently infected donors showed maximal expansion with single costimulatory molecules. Dual costimulation of T cells from recently infected donors or from healthy donors responding to influenza epitopes led to enhanced responses when the accumulation of cytokines was measured. However, accumulation of regulatory cytokines, particularly IFN-gamma, led to inhibition of further Ag-specific CD8 T cell expansion in the cultures. This inhibition was relieved by neutralization of IFN-gamma or of IFN-gamma, TNF, and IL-10. Thus, strong costimulation of T cells in vitro can lead to induction of regulatory cytokines at levels that limit further T cell expansion. In marked contrast, T cells from long-term (>4 years) infected HIV+ donors exhibited reduced Ag-specific CD8 T cell expansion, reduced CD4 T cell responses, and minimal cytokine accumulation. Dual costimulation with both 4-1BBL and B7.1 enhanced responses of T cells from long-term infected subjects to a level similar to that obtained with T cells from early in HIV infection. Experiments with purified CD8 T cells showed that B7.1 and 4-1BBL could act directly and synergistically on CD8 T cells. Taken together, these data suggest that 4-1BBL and B7.1 have additive or synergistic effects on HIV-specific CD8 T cell responses and represent a promising combination for therapeutic vaccination for HIV.

4-1BB Ligand↗
PubMed2004

Costimulatory ligand 4-1BBL (CD137L) as an efficient adjuvant for human antiviral cytotoxic T cell responses.

Effective adjuvants capable of inducing strong cytotoxic T cell responses in humans are lacking. In this study, we tested 4-1BBL as an adjuvant for activation of human memory antiviral CD8 T cell responses ex vivo. A recombinant replication-defective 4-1BBL adenovirus was used to convert autologous monocytes into efficient antigen-presenting cells after overnight incubation, bypassing the need to generate dendritic cells. Together with viral peptides, 4-1BBL led to robust memory responses of human Epstein-Barr virus- and influenza virus-specific cytotoxic T cells, with expansion of peptide-specific CD8 effector cells; up-regulation of Bcl-x(L), granzyme A, and perforin; enhanced cytotoxic activity; and increased cytokine production. The response was significant even at a 100-fold lower peptide dose, compared with responses obtained with control adenovirus. Adenovirus-delivered B7.1 also expanded and activated virus-specific CD8 T cells, but 4-1BBL was more effective in driving the T cells toward a more fully differentiated CD27(-) effector state. Thus, 4-1BBL is a promising adjuvant for human memory CD8 T cells and will likely be most effective in the boost phase of a prime-boost strategy.

4-1BB Ligand↗
PubMed2003

Costimulation of human CD28- T cells by 4-1BB ligand.

The T cell surface protein CD28 provides a critical costimulatory signal for T cell activation. With age, humans accumulate increasing numbers of CD28- T cells, and this loss of CD28 expression is exacerbated certain disease states, such as HIV infection, autoimmune conditions or cancer. It is unclear whether CD28- T cells represent terminally differentiated effector cells or whether they remain sensitive to costimulation by CD28-independent pathways. Here, we demonstrate that 4-1 BB ligand can costimulate human CD28- T cells, resulting in cell division, inflammatory cytokine production, increased perforin levels, enhancement of cytolytic effector function, as well as the up-regulation of the anti-apoptotic protein Bcl-X(L). Thus, human CD28- T cells can respond to costimulatory signals and as such become attractive targets for therapeutic intervention, particularly in chronic infectious and inflammatory diseases where large numbers of these cells accumulate.

4-1BB Ligand↗
PubMed2002

4-1BB ligand-mediated costimulation of human T cells induces CD4 and CD8 T cell expansion, cytokine production, and the development of cytolytic effector function.

4-1BB (CD137) is a costimulatory member of the TNFR family expressed on activated T cells. Its ligand, 4-1BBL, is expressed on activated APC. In the mouse, CD8 T cells are preferentially activated by agonistic anti-murine 4-1BB Abs. However, murine 4-1BBL can stimulate both CD4 and CD8 T cells. To date, there are only limited data on the effects of 4-1BBL on human T cell responses. To further understand the role of 4-1BBL in human T cell responses, we compared human CD4 and CD8 T cell responses to transfected human 4-1BBL plus TCR-mediated stimulation. Both human CD4 and CD8 T cells responded to 4-1BBL. The presence of 4-1BBL on the APC led to increased expansion, cytokine production, and the development of cytolytic effector function by human T cells. In unfractionated T cell cultures, CD4 and CD8 T cells could expand to a similar extent in response to signals through the TCR and 4-1BB, as measured by CFSE labeling and by quantitating T cell numbers in the cultures. In contrast to the results with total T cells, isolated CD8 T cells produced less IL-2 and expanded to a lesser extent than isolated CD4 T cells responding to 4-1BBL. Thus, 4-1BBL is most effective when both CD4 and CD8 T cells are included in the cultures. CD28 and 4-1BB were found to synergize in the induction of IL-2 by human T cells, and CTLA-Ig partially blocked 4-1BBL-dependent IL-2 production. However, a portion of the 4-1BBL-mediated effects were independent of CD28-B7 interaction.

4-1BB Ligand↗
PubMed2002

Generalized emissivity inverse problem.

Inverse problems have recently drawn considerable attention from the physics community due to of potential widespread applications [K. Chadan and P. C. Sabatier, Inverse Problems in Quantum Scattering Theory, 2nd ed. (Springer Verlag, Berlin, 1989)]. An inverse emissivity problem that determines the emissivity g(nu) from measurements of only the total radiated power J(T) has recently been studied [Tao Wen, DengMing Ming, Xianxi Dai, Jixin Dai, and William E. Evenson, Phys. Rev. E 63, 045601(R) (2001)]. In this paper, a new type of generalized emissivity and transmissivity inverse (GETI) problem is proposed. The present problem differs from our previous work on inverse problems by allowing the unknown (emissivity) function g(nu) to be temperature dependent as well as frequency dependent. Based on published experimental information, we have developed an exact solution formula for this GETI problem. A universal function set suggested for numerical calculation is shown to be robust, making this inversion method practical and convenient for realistic calculations.

Journal Article↗