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Biomedical subjects

B Xue

Publications and source records attributed to B Xue.

At least 37 records · Page 2Linked to original sources
PubMed1998

A clinical study on bing gan ling oral liquid for treatment of hepatitis C.

Based on the principles of cooling the blood to expel the pathogenic toxins and regulating the function of liver and activating the spleen in traditional Chinese medicine, 60 cases of chronic hepatitis C were treated with Bing Gan Ling (BGL), an oral liquid, which is composed mainly of Shuiniujiao (Cornu Bubali), Huzhang (Rhizoma Polygoni Cuspidati), Chishao (Radix Paeoniae Rubra), and Huangqi (Radix Astragali), etc. The total effective rate was 86.7%, which is considerably better than that of the control group (P < 0.01). The animal experiments and pathological studies suggest that the above-mentioned prescription has marked action of protecting the liver and lowering the activity of enzymes; and that it can ameliorate the acute liver injury induced by D-galactosamine.

Adult↗
PubMed1998

[Reversal effect of Ys-96, a bisbenzylisoquinoline, on adriamycin or vincristine resistance in human cancer cells in vitro].

OBJECTIVE: Reversal effect of Ys-96, a bisbenzylisoquinoline, on the resistance of human cancer cells to adriamycin or vincristine was studied in vitro. METHOD: In an in vitro culture system of human cancer cells MCF-7 and its adriamycin-resistant line MCF-7/Ad or KB and its vincristine-resistant line KBv200, the sensitivity(IC50) of the resistant cell lines to adriamycin or vincristine was evaluated with a MTT assay. RESULT: IC50 value of adriamycin or vincristine in combination with Ys-96 at a concentration of 1.00 mumol/L against MCF-7/Ad or KBv200 was found to be close to that of adriamycin alone or vincristine alone against the sensitive cell line MCF-7 or KB. CONCLUSION: The drug resistance of MCF-7/Ad or KBv200 could be essentially reversed by Ys-96 at a concentration of 1.00 mumol/L.

Benzylisoquinolines↗
PubMed1998

The agouti gene product inhibits lipolysis in human adipocytes via a Ca2+-dependent mechanism.

Overexpression of the murine agouti gene results in obesity. The human homologue of agouti is expressed primarily in human adipocytes, and we have shown recombinant agouti protein to increase adipocyte intracellular Ca2+([Ca2+]i) and thereby stimulate lipogenesis. However, since recent data demonstrate that increasing adipocyte [Ca2+]i may also inhibit lipolysis, we have investigated the role of agouti-induced [Ca2+]i increases in regulating lipolysis in human adipocytes. Short-term (1 h) exposure to recombinant agouti (100 nM) protein had no effect on basal lipolysis, although longer term treatment (24 h) caused a 60% decrease in basal lipolysis (P<0.0001). Short-term agouti treatment totally inhibited ACTH-induced lipolysis (P<0.05). Since melanocortin receptors (MCR) are involved in some actions of agouti, we next determined whether agouti's antilipolytic effect is exerted through competitive antagonism of the ACTH receptor (MCR-2). Forskolin (1 microM), an adenylate cyclase activator, induced a 48% increase in lipolysis in human adipocytes (P<0.05); this effect was reversed by 100 nM agouti (P<005), demonstrating that the antilipolytic effect of agouti is distal to the ACTH receptor. To determine the role of [Ca2+]i in the antilipolytic effect of agouti, human adipocytes were treated with KCl or arginine vasopressin to stimulate voltage- and receptor-stimulated Ca2+ influx, respectively. Both agents caused inhibition of forskolin-induced lipolysis (P<0.005). Furthermore, agouti's antilipolytic effect was also blocked by the Ca2+ channel blocker nitrendipine. These data demonstrate that agouti exerts a potent antilipolytic effect in human adipocytes via a Ca2+-dependent mechanism. This effect, combined with agouti-induced lipogenesis, represents a coordinate control of adipocyte lipid metabolism that may contribute to an agouti-induced obesity syndrome.

Adenosine Triphosphate↗
PubMed1997

The effect of aging on the immune response: influence of phosphatidylcholine-containing lipid on IgD-receptor expression and antibody formation.

It was reported previously that IgD-receptors (IgD-R) are expressed on both CD4+ and CD8+ human T cells and CD4+ murine T cells after exposure to oligomeric IgD, certain cytokines, or various pharmacological agents, as shown by rosetting with IgD-coated erythrocytes. Enhancement of antibody production is observed in mice after injection of oligomeric IgD and is mediated by these IgD-R+ T cells, while injection of monomeric IgD inhibits both IgD-R upregulation and augmentation of antibody responses induced by simultaneously injected oligomeric IgD. The effects of oligomeric IgD on IgD-R upregulation are lacking in aged mice. However, the oligomeric IgD induced enhanced antibody production can be transferred to aged mice with IgD-R+ T cells from young donors suggesting that the environment of the aged mouse supports the effector function of IgD-R+ T cells. We now report, in addition, that exposure to phosphatidylcholine (PC) and a PC-containing lipid mixture, AL721, is effective in causing IgD-R upregulation on T cells from both young and aged mice, and young humans. This effect can also be demonstrated in mice in vivo after administration of AL721. Moreover, this agent causes a two-fold enhancement of antibody production, as measured by PFC/spleen, to 4-hydroxy-5-iodo-3-nitrophenyl(acetyl)-Brucella abortus (NIP-BA) and NIP-horse red blood cells (RBC) in young and aged mice. There is no difference in the baseline membrane fluidity of lymphocytes from aged and young mice. Although PC causes an increase in membrane fluidity of lymphocytes from both young and old mice, and from humans, this effect on fluidity is not prevented by a protein kinase inhibitor, while PC's effect on IgD-R upregulation is prevented by the inhibitor. Moreover, no correlation was observed between IgD-R upregulation and membrane fluidity changes induced by AL721 administered in vivo. To evaluate the role of IgD-R induction in the augmentation of antibody production by phospholipids, the effect of monomeric IgD was investigated. The augmenting effect of AL721 on antibody production was prevented by a single injection of monomeric IgD at the time of antigen administration. We conclude that (1) PC-containing lipid mixtures are effective in enhancing antibody production in aged mice, (2) induction of IgD-R is responsible for the augmenting effects of AL721 on antibody production, and (3) monomeric IgD not only blocks the upregulation of IgD-R, as shown previously, but also the augmenting effect of previously upregulated IgD-R on T cells by preventing their interaction with surface IgD+ B cells.

Aging↗
PubMed1996

[The status quo and prospect of experimental study on channel tropism of Chinese herbal drugs].

The assay of metabolism and distribution of effective components of Chinese herbal drugs, microelement assay, pharmacodynamic assay and cAMP, cGMP assay are the essential methods usually used in the experimental study of channel tropism of Chinese herbal drugs. The problems of each method as well as the points for attention in the experimental study of channel tropism are discussed.

Animals↗
PubMed1996

[Effects of processing on specific toxicity and pharmacodynamics of radix Kansui, radix Achyranthis bidentatae and semen Armeniacae amarum].

The comparative toxicological researches on crude and processed drugs show that the activating action of Radix Kansui, Radix Achyranthis Bidentatae and Semen Armeniacae Amarum on EBV-EA can be decreased by processing. Processing can also decrease stimulating activity on mouse skin, inhibit tumor-promoting activity in two stage skin tumor promoting test and lapactic effect by Radix Kansui. Meanwhile the pharmacological effects of these drugs can be retained or increased by processing.

Animals↗
PubMed1996

[Antitussive, expectorant and anti-inflammatory effects of rhizoma Cynanchi stauntonii].

Experiments indicated that the ethanol extract and ether extract from Rhizoma Cynanchi Stauntonii showed obvious antitussive and expectorant effects in mice with stomach administration. The antitussive effect of ethanol extract was stronger than the expectorant effect. The water extract showed a certain expectorant effect but no marked antitussive effect with oral administration. Obvious anti-inflammatory effect was observed on croton oil-caused mouse ear swell with intraperitoneal injection.

Animals↗
PubMed1996

[Pharmacological comparative study on baiqian and baiwei].

The decoction of Cynanchum glaucescens and the ethanol extract of C. stauntonii show significant antitussive and expectorant actions. The decoctions of C. stauntonii or C. glaucescens have antiasthmatic and anti-inflammatory effects. The decoction of C. atratum has some expectorant effect but no antitussive or antiasthmatic actions. On the other hand, the decoction of C. versicolor cannot relieve cough nor sputum. The results indicate that both C. atratum and C. versicolor cannot be used as C. glaucescens or C. stauntonii.

Adolescent↗
PubMed1995

[Effect of processing on specific toxicity of radix Achyranthis bidentatae].

To activate Epstein-barr virus in Raji cells in vitro the lowest activation concentrations of ether extracts from Radix Achyranthis Bidentatae unprepared (I), stir-baked with wine (II) and stir-baked with salt (III) required were 0.8.20 and 0.16 micrograms/ml respectively. 5 microliters (equal to 250 mg herb weight)/ear of these extracts had inflammatory effect on mouse ear skin in 4 hours. Ethanol extract of I at concentration 0.04-125 mg/ml did not increase the chromosomal aberration rates in CHL cells. The decoctions of I, II, and III given orally at 15 g/kg x 3d showed no effect on micronucleus rates in mouse bone marrow. Ethanol extracts of I, II, and III at 10 g/kg x 10d did not show any evident antifertility action.

Animals↗
PubMed1995

[Antitussive, expectorant and anti-asthmatic effects of Cynanchum glaucescens (Decne.) Hand. -Mazz].

The water, ethanol and ether extracts from Cynanchum glaucescems administrated orally showed significant antitussive effect in ammonia-induced cough model in mice. The water and ethanol extracts had obvious expectorant effect. The filtered solution of water decoction injected intraperitoneally could effectively prevent guinea pigs from asthma induced by acetulcholine and histamine mixture, and also inhibit the ear inflammation in mice caused by croton oil. All these effects showed close dose-effect relationship.

Animals↗
PubMed1995

[Studies on comprehensive evaluation of toxic hazard in low-concentration benzene pollution].

Early adverse effects of exposure to benzene in a concentration less than 32 mg/m3 on the employees' health were comprehensively evaluated with WHO neurobehavioral core test battery, cytokinesis-block micronucleus assay for peripheral blood lymphocytes, determination of serum level of sialic acid and T-lymphocyte assay with alpha-naphthyl acetate esterase (ANAE) stain. Results revealed emotional irritability could be found in the exposed employees and 24% of them showed an abnormal percentage of micronuclei formation and increased serum level of sialic acid.

Adult↗
PubMed1995

[Antifebrile and anti-inflammatory effects of radix Cynanchi atrati].

The water extract of Radix Cynanchi Atrati used as intraperitoneal injection has been proved to have an obvious antifebrile++ effect on rat fever caused by 15% yeast suspension hypodermic injection as well as a significant anti-inflammatory effect. But the antiferbrile effect of its ethanol extract is not clear.

Animals↗
PubMed1993

Regulation of IgD-receptor expression on murine T cells. I. Characterization and metabolic requirements of the process leading to their expression.

Receptors for IgD (IgD-R) are found on murine CD4+ T cells and T cell clones. Previous work has shown that incubation with aggregated (but not monomeric) IgD causes the rapid upregulation of IgD-R and enables the T cells to respond with augmented helper function in antibody production. In the present study, IgD-R upregulation is shown to be (a) rapid, reaching plateau levels by 60 min, (b) independent of de novo protein or RNA synthesis, and (c) only slightly reduced at 4 degrees C. The IgD-R+ T cells present both before and after upregulation of IgD-R expression are predominantly resting T cells, whose ability to rosette with IgD-SRBC is inhibited by soluble IgD. The upregulation of IgD-R, even after overnight exposure to IgD, does not cause any detectable change in the expression of other T cell surface markers. Also characteristic of resting T cells is that they exhibit IgD-R in response to IL-2 and IL-4 only after overnight incubation with these cytokines, and fail to respond at all to IL-1. In contrast, cloned Th2 cells, expressing IL-1 and IL-2 receptors, show IgD-R upregulation after a 2-hr exposure to IL-1 or IL-2. GM-CSF, TNF-alpha, IL-6, and IL-10 do not modulate IgD-R expression. T hybridoma cells constitutively express much higher IgD-R levels than resting splenic T cells and can be stained with aggregated IgD followed by FITC-anti-IgD. Their levels of IgD-R expression decrease, as assayed both by rosetting and by staining, on 4-14 hr of incubation with tunicamycin or deoxynojirimycin, suggesting that N-linked glycosylation and oligosaccharide processing, respectively, are needed for continued expression of IgD-R. Tunicamycin-treated cells without detectable IgD-R on their surface still show IgD-binding protein in the cell extracts, suggesting that surface expression is more dependent on glycosylation of the IgD-R molecules than on the ability to bind IgD. Ca2+ ions are needed for optimal binding of IgD to IgD-R, in line with previous findings showing IgD-R to be lectin-like in binding carbohydrate rather than peptide regions of the IgD molecule.

Animals↗
PubMed1993

Regulation of IgD-receptor expression on murine T cells. II. Upregulation of IgD receptors is obtained after activation of various intracellular second-messenger systems; tyrosine kinase activity is required for the effect of IgD.

The presence of IgD receptors (IgD-R) on T cells during a primary response to antigen causes augmented antibody production and facilitates priming for a secondary response. Cross-linked, but not monomeric IgD leads to a rapid upregulation of these receptors on T cells. As shown in the present study, the rapid upregulation of IgD-specific receptors is also induced by cross-linking of T cell surface molecules known to mediate triggering of T cell activation, such as CD3, CD2, and Thy 1. Furthermore, IgD-R are also upregulated by pharmacologically active compounds that increase intracellular cAMP and by PMA/DiOG plus ionomycin, but not by either PMA or ionomycin alone. The upregulation of IgD-R by anti-CD3 is inhibited by both calphostin C and herbimycin A, while that due to DiOG plus ionomycin is only inhibited by calphostin C. Upregulation of IgD-R by increased cAMP is blocked by HA1004, but not by low concentrations of staurosporine or herbimycin A. IgD itself does not cause an increase in intracellular cAMP, protein kinase C translocation, influx of extracellular Ca2+, or a change in membrane potential. Relatively specific inhibitors of these activation pathways, HA1004, calphostin C, and neomycin, also fail to interfere with IgD-receptor upregulation by IgD itself. However, tyrosine kinase inhibitors, including herbimycin A, tyrphostin C11, and genistein, completely prevent the effect of IgD on IgD-R expression. Although an influx of Ca2+ is apparently not involved, a role for intracellular Ca2+ in the upregulation of IgD-R by IgD on T cells is indicated by the susceptibility to inhibition by BAPTA, W7, and FK520. We conclude that activation of at least three different second-messenger systems can cause IgD-R upregulation, but that the effect of IgD itself requires tyrosine kinase activity, perhaps in an intracellular Ca(2+)-dependent manner.

Animals↗
PubMed1988

Physiology of IgD. IX. Effect of IgD on immunoglobulin production in young and old mice.

Weekly i.p. injections of IgD from birth in (SJL X BALB/c)F1 mice were found to accelerate the development of IgG- and IgA-secreting cells and to increase the numbers of Ig-secreting cells of all isotypes in 17-28-day-old mice, but not in 7-10-day-old mice. Similarly, repeated weekly injections of IgD in normal adult BALB/c mice increased the numbers of reverse plaque-forming cells/spleen for all isotypes studied, including IgM, IgG1, IgG2, and IgA, but not for IgD itself. No such effect was observed in IgD-treated aged (20 months old) BALB/c mice. The absence of an effect of IgD on Ig secretion appeared to correlate with a lack of induction of receptors for IgD on T cells of the host, both in 7-10-day-old and in aged mice. In 7-10-day-old mice this lack of induction appeared due to their very low numbers of L3T4+ T cells. A comparison was made between the effect of a single injection of IgD or lipopolysaccharide (LPS) on numbers of Ig-secreting cells in the spleen determined 1-7 days after injection. Both agents caused increases, but the increase in IgM-producing cells was much greater after LPS (day 4), while IgD caused a relatively greater increase in IgG2 and IgA (days 4-7). Increases in IgG1 and IgG3-producing cells induced by LPS and IgD were of similar magnitude (days 6-7). IgD production, however, was not increased. The number of cells producing antibody of anti-trinitrophenyl (TNP) specificity was enhanced by LPS (day 4), but not by a single injection of IgD, although more than one injection of IgD caused a significant increase in anti-TNP-producing cells above background. LPS, but not IgD, caused B cell proliferation in vitro in the presence or absence of gamma-irradiated T delta cells. However, in vivo, IgD injections caused a significant increase in the percentage of lymphoid follicles with germinal centers in lymph nodes from 17-21-day-old and normal adult mice, but not in 7-10-day-old or aged mice. Such an effect was also absent in 24-28-day-old mice, where germinal center development, even in untreated mice, was very high.

Aging↗