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C Wang

Publications and source records attributed to C Wang.

At least 199 records · Page 11Linked to original sources

Feeding inhibition by urocortin in the rat hypothalamic paraventricular nucleus.

Ventricular administration of urocortin (UCN) inhibits feeding, but specific site(s) of UCN action are unknown. In the current studies we examined the effect of UCN in the hypothalamic paraventricular nucleus (PVN) on feeding. We tested UCN administered into the PVN in several paradigms: deprivation-induced, nocturnal, and neuropeptide Y (NPY)-induced feeding. We compared the effect of equimolar doses of UCN and corticotrophin releasing hormone (CRH) on NPY-induced and nocturnal feeding, determined whether UCN in the PVN produced a conditioned taste aversion (CTA) and induced changes in c-Fos immunoreactivity (c-Fos-ir) after UCN and NPY administration in the PVN. UCN in the PVN significantly decreased NPY and nocturnal and deprivation-induced feeding at doses of 1, 10, and 100 pmol, respectively. UCN anorectic effects lasted longer than those attributed to CRH. Ten and thirty picomoles UCN did not induce a CTA, whereas 100 pmol UCN produced a CTA. UCN (100 pmol) in the PVN neither increased c-Fos-ir in any brain region assayed nor altered c-Fos-ir patterns resulting from PVN NPY administration. These data suggest the hypothalamic PVN as a site of UCN action.

Animals↗

Adrenomedullin gene delivery attenuates renal damage and cardiac hypertrophy in Goldblatt hypertensive rats.

Adrenomedullin (AM) is a potent vasodilator and natriuretic peptide that plays an important role in cardiovascular function. In this study, we employed a somatic gene delivery approach to explore its potential protective role in renovascular hypertension. A single tail vein injection of adenovirus harboring the human AM gene significantly blunted a blood pressure increase that lasted for more than 3 wk in two-kidney one-clip (2K1C) hypertensive rats. The expression of human AM mRNA was detected in the kidney, adrenal gland, heart, lung, and liver, and immunoreactive human AM was detected in the plasma and urine of 2K1C rats after human AM gene delivery. A maximal blood pressure difference of 28 mmHg was observed 10 days after AM gene delivery, compared with that in rats injected with the control virus carrying the LacZ gene. Human AM gene delivery significantly attenuated increases in the ratio of left ventricular weight to heart weight, cardiomyocyte diameter, and fibrosis in the heart, as well as glomerular sclerosis, tubular injuries, and protein casts in the kidney. The beneficial effects of AM gene delivery were accompanied by increased urinary cAMP levels, indicating activation of AM receptors. These findings provide new insights into the role of AM in renovascular hypertension and may have significance in therapeutic applications in cardiovascular diseases.

Adenoviridae↗

Role of NMDA, non-NMDA, and GABA receptors in signal propagation in the amygdala formation.

Although the synaptic physiology of the amygdala has been studied with single neuron recordings, the properties of the networks between the various nuclei have resisted characterization because of the limitations of field recording in a neuronally diffuse structure. We addressed this issue in the rat amygdala complex in vitro by using a photodiode array coupled with a voltage-sensitive dye. Low-intensity single pulse stimulation of the lateral amygdala nucleus produced a complex multi-phasic potential. This signal propagated to the basolateral nucleus and the amygdalostriatal transition zone but not to the central nucleus. The local potential, which depended on both synaptic responses and activation of voltage-dependent ion channels, was reduced in amplitude by the non-N-methyl-D-aspartate (non-NMDA) glutamate receptor antagonist 6,7-dinitroquinoxaline (DNQX) and reduced to a lesser extent by the NMDA glutamate receptor antagonist D-2-amino-5-phosphonovaleric acid (D-APV). We next characterized the less complex signals that propagated to more distal regions with or without the addition of the GABA receptor antagonist bicuculline (BIC). BIC alone greatly increased the signal propagation and permitted activation of previously silent areas within the amygdala. DNQX blocked signal propagation to amygdala regions outside of La, even in the presence of BIC, whereas D-APV had minimal effects on these distal signals. These data represent several novel findings: the characterization of the multi-component potential near the site of stimulation, the gating of signal propagation within the amygdala by GABAergic inhibition, the critical role of non-NMDA receptor-mediated depolarization in signal propagation, and the lack of a role for NMDA receptors in maintaining propagation.

2-Amino-5-phosphonovalerate↗

Aging-related increased expression of inducible nitric oxide synthase and cytotoxicity markers in rat hypothalamic regions associated with male reproductive function.

UNLABELLED: We have previously demonstrated that the inducible nitric oxide synthase (iNOS) protein and total NOS activity increase in the hypothalamus and other regions of the male rat brain during aging. We have now tested the hypothesis that increased iNOS results in excessive nitric oxide (NO) and peroxynitrite production, and leads to increased apoptosis in CNS cells, including the GnRH and oxytocin hypothalamic neurons involved in the control of male reproductive function. Young (3-month-old) and old (24-month-old) male Brown Norway rats (n = 6) were perfused with 4% formalin. Adjacent coronal paraffin-embedded sections (5 microm) of preoptic area (POA), supraoptic nucleus (SON), paraventricular nucleus (PVN), and arcuate nucleus (ARC) of the hypothalamus were immunostained with antibodies for iNOS, neuronal NOS (nNOS), and nitrotyrosine (a marker of peroxynitrite formation). The intensity of immunostaining was measured using a densitometric image analysis system. Apoptosis was determined by the TUNEL assay. Double immunofluorescence staining with confocal laser scanning microscopy was used for co-localization studies. A significant increase in the iNOS immunostaining measured as optical density (OD) was found in the old compared to the young animals (SON: 0.32 +/- 0.02 vs. 0.23 +/- 0.03, p < 0.05; PVN: 0.34 +/- 0.03 vs. 0.07 +/- 0.05, p < 0.001; POA: 0.18 +/- 0.02 vs. 0.01 +/- 0.02, p < 0.001). Aging did not affect nNOS expression. Nitrotyrosine was elevated in the hypothalamic regions of old compared to young rats (SON: 0.32 +/- 0.05 vs. 0.10 +/- 0.04, p < 0.05; PVN: 0.32 +/- 0.04 vs. 0.13 +/- 0.03, p < 0.01; POA: 0.72 +/- 0.06 vs. 0.03 +/- 0.003, p < 0.001). Increased nitrotyrosine was accompanied by an elevation of the apoptotic index in the old rats (SON: 11.01 +/- 3.33 vs. 0.57 +/- 0.50, p < 0.001; PVN: 3.08 +/- 1.12 vs. 0.42 +/- 0.32; POA: 6.60 +/- 1.93 vs. 0.18 +/- 0.17, p < 0.01; ARC: 0.001 +/- 0.0001 vs. 4.33 +/- 2.33). iNOS staining co-localized with GnRH and oxytocin staining. IN CONCLUSION: The aging-related iNOS increased expression in the hypothalamus of the male rat affects regions known to control the synthesis and release of GnRH (POA, ARC) and oxytocin (PVN, SON), and the factors regulating penile erection (POA, and PVN). These observations suggest that iNOS may play a role in the reduction in GnRH and oxytocin neuronal secretion resulting in reproductive dysfunctions such as lowered serum testosterone, hypospermatogenesis, and diminished copulatory function in the aging male animal.

Aging↗

Surgical treatment of intractable epilepsy combined with bipolar electrocoagulation on functional cortex.

OBJECTIVE: Resecting epileptogenic foci combined with bipolar electrocoagulation of functional cortex has been successfully used to treat intractable epilepsy. METHOD: 124 cases with intractable epilepsy have been treated from 1996 to 1999, 75 cases with temporal lobe epilepsy and 48 cases with extra-temporal lobe epilepsy, and one case with infantile hemiplegia. Electrocorticography (ECoG) was used pre- and postoperatively. 108 cases were followed-up from one to three years. RESULTS: The general efficiency of bipolar electrocoagulation on functional cortex (BCFC) for epilepsy is 91.7%. The pathological features indicate that the damage by coagulation of the cortex is only in the supra- and infra-granular layers, similar to multiple subpial transection (MST). CONCLUSION: When the epileptogenic foci are located in functional cortex, the method of resecting the foci combined with BCFC has been effective and improves the results greatly. BCFC is safe and easy to use.

Adolescent↗

A novel method for enzyme immobilization: direct encapsulation of acid phosphatase in nanoporous silica host materials.

Immobilization of acid phosphatase (ACP) in mesoporous or, more generally, nanoporous silica has been accomplished via the sol-gel reactions of tetramethyl orthosilicate in the presence of ACP and of D-glucose (DG) as a nonsurfactant template, which is subsequently removed by water extraction after the formation of nanocomposite gels. Characterization of the silica host after the removal of DG shows that the pore size and volume generally increase with the DG content. At high DG contents, the silica hosts are nanoporous with interconnected nanoscaled pores/channels of regular diameter (e.g., 3.4 nm). Catalytic activity of ACP encapsulated in nanoporous hosts is significantly improved over that in microporous host prepared in the absence of DG. The apparent enzymatic activity at various pH values and substrate concentrations correlates well with the nanostructures of the host matrices. As the DG content is increased in the synthesis, the activity tends to increase. At a DG content of 42-60 wt%, the samples exhibit activities about triple that of the template-free control. These and other results from enzymatic kinetic studies suggest that the increase in the pore size and volume facilitates the transport of the substrate and product molecules in the host matrices, leading to the observed increase in activity. The thermal stability of ACP is remarkably improved upon immobilization. There is no detectable leakage of ACP from the host matrices and the biogels are reuseable. This study provides a useful protocol for the development of nanotechnology for various biocatalysts and biosensors.

Acid Phosphatase↗

In situ hybridization and immunohistochemical analysis of cytochrome P450 1B1 expression in human normal tissues.

Cytochrome P450 1B1 (CYP1B1) is a recently cloned dioxin-inducible form of the cytochrome P450 supergene family of xenobiotic-metabolizing enzymes. CYP1B1 is constitutively expressed mainly in extrahepatic tissues and is inducible by aryl hydrocarbon receptor ligands. Human CYP1B1 is involved in activation of chemically diverse human procarcinogens, including polycyclic aromatic hydrocarbons and some aromatic amines, as well as the endogenous hormone 17 beta-estradiol. The metabolism of 17 beta-estradiol by CYP1B1 forms 4-hydroxyestradiol, a product believed to be important in estrogen-induced carcinogenesis. Although the distribution of CYP1B1 mRNA and protein in a number of human normal tissues has been well documented, neither the cells expressing CYP1B1 in individual tissue nor the intracellular localization of the enzyme has been thoroughly characterized. In this study, using nonradioactive in situ hybridization and immunohistochemistry, we examined the cellular localization of CYP1B1 mRNA and protein in a range of human normal tissues. CYP1B1 mRNA and protein were expressed in most samples of parenchymal and stromal tissue from brain, kidney, prostate, breast, cervix, uterus, ovary, and lymph nodes. In most tissues, CYP1B1 immunostaining was nuclear. However, in tubule cells of kidney and secretory cells of mammary gland, immunoreactivity for CYP1B1 protein was found in both nucleus and cytoplasm. This study demonstrates for the first time the nuclear localization of CYP1B1 protein. Moreover, the constitutive expression and wide distribution of CYP1B1 mRNA and protein in many human normal tissues suggest functional roles for CYP1B1 in the bioactivation of xenobiotic procarcinogens and endogenous substrates such as estrogens. (J Histochem Cytochem 49:229-236, 2001)

Aryl Hydrocarbon Hydroxylases↗

XXY male mice: an experimental model for Klinefelter syndrome.

Klinefelter syndrome (47,XXY) is the most common sex chromosome aneuploidy in men. Thus, it is important to establish an experimental animal model to explore its underlying molecular mechanisms. Mice with a 41,XXY karyotype were produced by mating wild-type male mice with chimeric female mice carrying male embryonic stem cells. The objectives of the present study were to characterize the testicular phenotype of adult XXY mice and to examine the ontogeny of loss of germ cells in juvenile XXY mice. In the first experiment the testicular phenotypes of four adult XXY mice and four littermate controls (40,XY) were studied. XXY mice were identified by either Southern hybridization or karyotyping and were further confirmed by fluorescence in situ hybridization. The results showed that the testis weights of adult XXY mice (0.02 +/- 0.01 g) were dramatically decreased compared with those of the controls (0.11 +/- 0.01 g). Although no significant differences were apparent in plasma testosterone levels, the mean plasma LH and FSH levels were elevated in adult XXY mice compared with controls. The testicular histology of adult XXY mice showed small seminiferous tubules with varying degrees of intraepithelial vacuolization and a complete absence of germ cells. Hypertrophy and hyperplasia of Leydig cells were observed in the interstitium. Electron microscopic examination showed Sertoli cells containing scanty amounts of cytoplasm and irregular nuclei with prominent nucleoli. The junctional region between Sertoli cells appeared normal. In some tubules, nests of apparently degenerating Sertoli cells were found. In the second experiment the ontogeny of germ cell loss in juvenile XXY mice and their littermate controls was studied. Spermatogonia were found and appeared to be morphologically normal in juvenile XXY mice. Progressive loss of germ cells occurred within 10 days after birth. This resulted in the absence of germ cells in the adult XXY mice. We conclude that a progressive loss of germ cells occurring in early postnatal life results in the complete absence of germ cells in adult XXY mice. The XXY mouse provides an experimental model for its human XXY counterpart, Klinefelter syndrome.

Animals↗

Overexpression of parathyroid hormone-related protein enhances apoptosis in the rat intestinal cell line, IEC-6.

We used the rat intestinal cell line, IEC-6, to study potential effects of overexpression of PTH-related protein (PTHrP) on apoptosis. A clonal line of PTHrP-overexpressing cells was established by stably transfecting parental cells with PTHrP complementary DNA in a sense orientation (sense). A similarly transfected line stably, transfected with empty vector, served as control (vector). Immunoreactive PTHrP, measured in culture medium, showed that sense cells secreted approximately 30 times as much PTHrP as did vector control cells. Apoptosis induced by serum withdrawal was evaluated by several methods. DNA laddering was demonstrable in sense-transfected cells as early as 12 h after serum withdrawal but not until later time points in vector-transfected control cells. Flow cytometric analysis of propidium iodide-stained cells showed a greater increase in the sub-G1 (apoptotic) population in sense cells, compared with vector. Fluorescent microscopy with Hoechst 33258 dye showed increased nuclear fragmentation and condensation in sense cells. Studies of apoptotic gene expression by ribonuclease protection assay, and protein by Western blot analysis, showed an enhanced ratio of Bax to Bcl-x(L) in sense cells. Mutation of the PTHrP nuclear localization amino acid sequence negated the ability of PTHrP to enhance apoptosis.

Animals↗

Cyclin D1 binds the androgen receptor and regulates hormone-dependent signaling in a p300/CBP-associated factor (P/CAF)-dependent manner.

The androgen receptor (AR) is a ligand-regulated member of the nuclear receptor superfamily. The cyclin D1 gene product, which encodes the regulatory subunit of holoenzymes that phosphorylate the retinoblastoma protein (pRB), promotes cellular proliferation and inhibits cellular differentiation in several different cell types. Herein the cyclin D1 gene product inhibited ligand-induced AR- enhancer function through a pRB-independent mechanism requiring the cyclin D1 carboxyl terminus. The histone acetyltransferase activity of P/CAF (p300/CBP associated factor) rescued cyclin D1-mediated AR trans-repression. Cyclin D1 and the AR both bound to similar domains of P/CAF, and cyclin D1 displaced binding of the AR to P/CAF in vitro. These studies suggest cyclin D1 binding to the AR may repress ligand-dependent AR activity by directly competing for P/CAF binding.

Acetyltransferases↗

Composition, characteristic and activity of rare earth element-bound polysaccharide from tea.

The compositions and structural characteristics of rare earth elements-bound polysaccharides from tea (REE-TPS) were studied with the methods of Inductively Coupled Plasma Mass Spectrometry (ICP-MS), Gas Chromatography (GC) and Extended X-ray Absorption Fine Structure (EXAFS) spectroscopy. The results show that polysaccharide from tea (TPS) was a sort of glycoprotein and coordinated with Rare Earth Elements (REE) closely. The sugar fraction was composed of Rha, Ara, Xyl, Fuc, Glc, and Gal. There existed almost all natural amino acids with Glx, Asx, and Hyp as the major parts in the protein fraction. The REEs in REE-TPS were mainly composed of La, Ce, and Nd, especially, more than 75% of them was La. The coordination atom of the first coordination shell of La in REE-TPS was oxygen, the coordination number of which was 6, and the average distance between the atoms was 2.52 A. The second shell was formed from sulfur atoms, the coordination number and the average distance were 3 and 2.91 A, respectively. The bio-experiments show that REE-TPS could decrease the content of blood glucose in mice significantly.

Animals↗

Presence of antibody against the inducible Hsp71 in patients with acute heat-induced illness.

Antibodies against heat shock or stress proteins (Hsps) have been reported in a number of diseases in which they may be involved in the pathogenesis of the disease or may be of use for prognosis. Heat-induced diseases, such as heat cramps, heat exhaustion, or heat stroke, are frequent in hot working or living environments. There are still few investigations on the presence and possible significance of autoantibodies against Hsps in heat-induced illnesses. Using an immunoblotting technique with recombinant human Hsps, we analyzed the presence and titers of antibodies against Hsp60, Hsp71, and Hsp90alpha, and Hsp90beta in a group of 42 young male patients who presented with acute heat-induced illness during training. We also examined the presence of antibody against Hsp71 in a second group of 57 patients with acute heat-induced illness and measured the changes in titers of anti-Hsp71 antibodies in 9 patients hospitalized by emergency physicians. In the first group of young persons exercising in a hot environment, the occurrence of antibodies against Hsp71 and Hsp90alpha was significantly higher among individuals with symptoms of heat-induced illness (P < 0.05) than in the matched group of nonaffected exercising individuals. Moreover titers of antibody against Hsp71 were higher in individuals of the severe and mild heat-induced illness groups, the highest titer being found in the most severe cases. The results from the second group of 57 heat-affected patients exposed to extreme heat were similar. Again, patients with the more severe heat-induced symptoms showed a significantly higher incidence of antibodies to Hsp71 than controls and the titer of anti-Hsp71 was higher in the severely affected group. Finally, in a study of 9 patients, it was observed that the titer of anti-Hsp71 decreased during recovery from severe heat symptoms. These results suggest that measurement of antibodies to Hsps may be useful in assessing how individuals are responding to abnormal stress within their living and working environment and may be used as one biomarker to evaluate their susceptibility to heat-induced diseases.

Adolescent↗

Concentrations and flux of rare earth elements in a semifield plot as influenced by their agricultural application.

The concentrations of rare earth elements (REs) in atmospheric particles, soil, soil water, surface runoff, and different parts of corn in an experimental plot in the suburb of Beijing, China were measured and the flux of REs was estimated. The concentration of REs in air particles with diameter less than 10 microm is 36 ng/m3 and, by ratio analysis, the origin of REs in the atmosphere was likely local soil. The concentration of soluble REs is 0.69 microg/L in rainwater, 5-7 microg/L in surface runoff, as well as 1-4 microg/L in soil water and the application of RE mixture has no observed influences on their concentrations. The concentration of soluble REs in surface runoff and soil water was dominated by aqueous-solid-phase partitioning. By estimation of the flux, most of the REs applied will remain in the soil phase and continued application of REs will cause an accumulation of REs in agricultural soil.

China↗

A comparison of pitfall traps with bait traps for studying leaf litter ant communities.

A comparison of pitfall traps with bait traps for sampling leaf litter ants was studied in oak-dominated mixed forests during 1995-1997. A total of 31,732 ants were collected from pitfall traps and 54,694 ants were collected from bait traps. They belonged to four subfamilies, 17 genera, and 32 species. Bait traps caught 29 species, whereas pitfall traps caught 31 species. Bait traps attracted one species not found in pitfall traps, but missed three of the species collected with pitfall traps. Collections from the two sampling methods showed differences in species richness, relative abundance, diversity, and species accumulation curves. Pitfall traps caught significantly more ant species per plot than did bait traps. The ant species diversity obtained from pitfall traps was higher than that from bait traps. Bait traps took a much longer time to complete an estimate of species richness than did pitfall traps. Little information was added to pitfall trapping results by the bait trapping method. The results suggested that the pitfall trapping method is superior to the bait trapping method for leaf litter ant studies. Species accumulation curves showed that sampling of 2,192+/-532 ants from six plots by pitfall traps provided a good estimation of ant species richness under the conditions of this study.

Animals↗

DNA (cytosine) methyltransferase overexpression is associated with acquired drug resistance of murine neuroblastoma cells.

We have previously reported that C-1300 murine neuroblastoma (rMNB) cells made resistant to the nucleoside analogue, (Z)-5'-fluoro-4', 5'-didehydro-5'deoxyadenosine (MDL), an irreversible inhibitor of S-adenosylhomocysteine (AdoHcy) hydrolase have an increased expression of the S-adenosylmethionine (AdoMet) synthetase gene. Results of the immunoblot analysis of DNA (cytosine) methyltransferase with anti-human DNA (cytosine) methyltransferase specific polyclonal antibody demonstrated a significant increase ( approximately 2-fold, p<0.01) in expression of DNA (cytosine) methyltransferase protein in rMNB/MDL cells compared to wild-type C1300 MNB (wMNB) cells. To rule out the possibility that multidrug resistance (MDR) genes are involved in development of acquired drug resistance in murine neuroblastoma (rMNB/MDL) cells made resistant to MDL, the expression of Mdr1a, Mdr1b, Mdr2 (multidrug resistance/P-glycoprotein), and Mrp-1 (multidrug resistance associated protein) was examined in rMNB-MDL cells. The analysis of Mdr and Mrp-1 expression was performed by RT-PCR using PCR specific primers to respective genes. No significant difference was observed in the expression of MDR1a, Mdr1b and Mrp-1 genes between wMNB and rMNB-MDL cells, however, a slight decrease was noticed in Mdr1 expression in some samples. Expression of the Mdr2 (human MDR3) gene, which is not associated with the acquired drug resistance phenotype, was significantly decreased in rMNB-MDL cells. These findings were also confirmed by the immunoblot analyses using specific monoclonal antibodies to Mdr1/3 proteins. Expression of N-Myc gene--a prognostic factor in neuroblastoma tumors was also not altered in rMNB-MDL cells. Results of the present study suggest that acquired drug resistance in rMNB-MDL cells to MDL is associated to the overexpression of DNA (cytosine) methyltransferase, and could be due to genetic or epigenetic changes in particular to DNA hypermethylation in response to an increased AdoMet synthetase gene expression.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

Pharmacological characterization of locomotor sensitization induced by chronic phencyclidine administration.

Phencyclidine (PCP) administration in rats acutely in high doses or chronically in lower doses causes neurotoxicity characterized by neuronal vacuolization and apoptotic neuronal death, respectively. The purpose of this study was to determine whether drugs that previously had been reported to prevent either type of neurotoxicity were also able to prevent locomotor sensitization following chronic PCP administration. PCP (5 or 20 mg/kg) was administered once a day for 5 days following drug pretreatment. After withdrawal, rats were challenged with 3.2 mg/kg PCP and locomotor activity was assessed. Haloperidol and clozapine significantly attenuated sensitization elicited by PCP (20 mg/kg). The D(1)-like antagonist SCH23390 was much less effective than clozapine, showing a marginal inhibition. Risperidone, a D(2)/serotonin (5-HT(2)) antagonist, also resulted in a marginal attenuation of 15%. Ketanserin, a 5-HT(2) antagonist, had no effect. Atropine retarded sensitization by 35% and (+)-sulpiride caused a 50% reduction. The AMPA/kainate antagonist, 6,7-dinitroquinoxaline-2,3-dione, had no effect, but barbital sodium reduced sensitization by 54%. These data suggest that gamma-aminobutyric acid A, D(2), and muscarinic receptors play a major role in the complex pathway underlying sensitization to PCP, whereas D(1), 5-HT(2) and AMPA receptors have little or no relevance in the behavioral sensitization produced by 20 mg/kg PCP. In a model using 5 mg/kg PCP, the effects of sulpiride and SCH23390 replicated those observed with 20 mg/kg PCP and further showed that acute locomotor activation is not a strict requirement for the development of sensitization. These data argue that there is overlap, but nonidentity, between the mechanisms underlying PCP-induced sensitization and neurotoxicity.

Animals↗

mRNA and protein expression of Fas associated death domain protein in apoptosic hepatocyte induced by tumor necrosis factor-alpha.

OBJECTIVE: To study the expression of protein and mRNA of Fas associated death domain protein (FADD) in the apoptosic hepatocyte induced by D-galactosamine (GalN) and TNF-alpha. METHODS: Fulminant hepatic failure (FHF) was induced by injection of GalN into sensitized BALB/c mice by TNF-alpha. Hepatocyte apoptosis was examined by electric microscopy, in site end labeling (ISEL) and DNA electrophoresis on 1.5% agarose gel. The expression of protein and mRNA of FADD were detected by immunohistochemistry and PT-PCR. RESULTS: GalN/TNF-alpha may induce hepatocyte apoptosis, necrosis and liver failure. The expression of protein and mRNA of FADD were positively correlative with the apoptosic hepatocytes. CONCLUSION: TNF-alpha induces hepatocyte apoptosis by up regulation expression of FADD protein.

Adaptor Proteins, Signal Transducing↗