Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclooxygenase (COX) inhibitors were regarded as anticarcinogenic agents for lung cancer at least partly via PGE2; but these were based on cytokin stimulation experiment on A549 cell. In order to clarify whether COX inhibitors directly inhibit A549 cell, three COX inhibitors, NS398 (selective COX-2 inhibitor), SC560 (selective COX-1 inhibitor), and acetyl salicylic acid (ASA, non-selective COX inhibitor), were studied. NS398, and ASA, can inhibit PGE2 generation via COX-2 inhibition. The viability of A549 cell was assayed by MTT. However, without cytokin stimulation, all the three inhibitors (NS398 0.2-20 microM; SC560 1.0-100 nM; ASA 0.01-1.0 mM) were not able to inhibit A549 cell proliferation, in the other way round, NS398 promoted cell growth. And arachidonic acid (AA) and lipopolysaccharide (LPS) did not disturb the property of its growth. These data suggested that without cytokin stimulation, COX and PGE2 may not be the kernel molecules involved in A549 cell proliferation, and COX inhibitors could not inhibit A549 cell growth directly.
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PMID:Cyclooxygenase inhibitors not inhibit resting lung cancer A549 cell proliferation. 1661 38

Fumonisin B1 (FB1) is a mycotoxin produced by the fungus Fusarium verticillioides (formerly Fusarium moniliforme) and is found in diverse crops such as corn, wheat, and barley. Many diseases linked to FB1, such as porcine pulmonary edema, rat hepatic cancer, and equine leukoencephalomalacia, indicate a compromised immune system. The purpose of this study was to determine whether FB1 altered immunological responses in various cell populations of Single Comb White Leghorn chicks. Cells collected for this study were obtained from those immunological organs with well-defined responses (i.e., spleen, thymus, and blood). Cell populations were exposed to 5 to 50 microg/mL FB1 in vitro for 24 to 72 h, and viability and mitogenic response were evaluated. The effects of FB1 on the mitogenic response were evaluated in cell populations from the spleen and blood stimulated with the mitogens, lipopolysaccharide, concanavalin A, and pokeweed mitogen and in thymocytes stimulated with concanavalin A. The 3-(4,5-dimethylthazol-2-yl)-diphenyl-2H-tetrazolium bromide (MTT) reduction assay was used to assess viability and mitogenic response. Fumonisin B1 decreased spleen cell viability and mitogenic response, albeit the degree of decrease varied with mitogen and time of exposure. Fumonisin B1 increased number of viable thymic cells at 50 microg/mL but had no effect on the mitogenic response of thymocytes. Fumonisin B1 had no effect on blood lymphocyte viability or mitogenic response.
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PMID:The effects of fumonisin B1 on viability and mitogenic response of avian immune cells. 1677 70

Ginsenoside Rd (Rd), a saponin isolated from the roots of panax notoginseng, was evaluated for inducing Th1 or Th2 immune responses in mice against ovalbumin (OVA). ICR mice were immunized subcutaneously with OVA 100 microg alone or with OVA 100 microg dissolved in saline containing alum (200 microg), or Rd (10, 25 or 50 microg) on days 1 and 15. Two weeks later (day 28), concanavalin A (Con A)-, lipopolysaccharide (LPS)- and OVA-stimulated splenocyte proliferation was determined using MTT assay, and OVA-specific antibody titers and levels of cytokines in serum were measured by ELISA and microparticle-based flow cytometric immunoassay, as well as peripheral blood T-lymphocyte subsets analyzed using flow cytometer. Rd significantly enhanced the Con A-, LPS-, and OVA-induced splenocyte proliferation in the OVA-immunized mice. OVA-specific IgG, IgG1, and IgG2b antibody titers in serum were significantly enhanced by Rd compared with OVA control group. Meanwhile, Rd also significantly promoted the production of the Th1 and Th2 cytokines in OVA-immunized mice. Further, the effects of Rd on expression of cytokine mRNA in Con A-stimulated mice splenocytes were evaluated by RT-PCR analysis. Rd significantly enhanced the interleukin-2 (IL-2), interferon-gamma (IFN-gamma), IL-4, and IL-10 mRNA expression in mice splenocyte induced by Con A. These results suggested that Rd had immunological adjuvant activity, and elicited a Th1 and Th2 immune response by regulating production and gene expression of Th1 cytokines and Th2 cytokines.
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PMID:Ginsenoside Rd elicits Th1 and Th2 immune responses to ovalbumin in mice. 1695 May 47

The main objective of this study was to develop a nondestructive reporter system for assessing the response of human cells contained within a three-dimensional (3D) tissue-engineered construct to exogenous stress. Dermal fibroblasts were transiently transfected with a reporter construct linked to nuclear factor kappaB (NF-kappaB) activation which led to expression of a nonstable form of enhanced green fluorescent protein (d2EGFP) after stimulation. This led to a temporary production of fluorescence, which could be readily detected but was not intrinsically toxic, as cells were able to metabolize the initial cycle of d2EGFP produced. This permitted the model to be used for restimulation post recovery. To investigate the performance and predictive ability of this method for assessing cellular response to stress in 3D, we used a range of compounds known to have pro-inflammatory or oxidative properties. Tumor necrosis factor-alpha (TNF-alpha) and interleukin-1-beta (IL-1beta) were selected for having a direct cytokine action; lipopolysaccharide (LPS) was selected for modeling bacterial-mediated inflammation; and hydrogen peroxide was selected as a crude method for delivering an oxidative stress. Transfected cells were stimulated with the above compounds in 3D and the synthesis of d2EGFP was detected as a measure of NF-kappaB activation. The resultant fluorescence was scored using a series of photomicrographs taken by epifluorescence microscopy. All agents activated NF-kappaB when cells were grown in 3D scaffolds but did not cause any significant reduction in cell viability as measured by a standard MTT-ESTA viability test. Parallel NF-kappaB activation and MTT measurements was also conducted in two-dimension (2D) and confirmed findings in 3D. The 3D model described using a fluorescent reporter gene is a highly sensitive and reliable method for detecting cellular stress and represents a key step in developing tissue engineering models with the potential for screening pharmaceutical and cosmetic compounds, as an alternative to existing in vitro and in vivo methods.
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PMID:Real-time detection of stress in 3D tissue-engineered constructs using NF-kappaB activation in transiently transfected human dermal fibroblast cells. 1743 89

Peloruside A (peloruside) is a naturally occurring compound isolated from a New Zealand marine sponge that, like the anticancer drug paclitaxel, stabilizes microtubules and inhibits mitosis. Paclitaxel is known to induce a proinflammatory response in murine macrophages; whereas, peloruside has never been tested for its immunomodulatory effects in these cells. Although the antimitotic effects of the two drugs appear to be similar, we found that peloruside, unlike paclitaxel, does not induce murine macrophages to produce the proinflammatory mediators interleukin-12p40 (IL-12p40), tumor necrosis factor-alpha (TNF-alpha), and nitric oxide. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction assay confirmed that the absence of cytokine production was not caused by cytotoxicity in these nondividing cells. Additionally, there was no effect on unstimulated splenocytes; whereas, both compounds inhibited proliferation after concanalavin A (Con A) stimulation. Finally, there was a significant decrease in TNF-alpha and nitric oxide but not IL-12p40 when macrophages were cultured with lipopolysaccharide (LPS) and either paclitaxel or peloruside. These results suggest that peloruside may prove to be an effective anti-inflammatory treatment, since it does not induce the production of proinflammatory mediators yet can downregulate TNF-alpha and nitric oxide production by LPS-stimulated macrophages, as well as inhibit lymphocyte proliferation.
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PMID:Peloruside A, an antimitotic agent, specifically decreases tumor necrosis factor-alpha production by lipopolysaccharide-stimulated murine macrophages. 1746 56

Glomerulosclerosis is a common disorder in many types of chronic kidney diseases. Previous studies have shown that glomerular mesangial cells (MCs) play an important role in the pathogenesis of glomerulosclerosis. The ability of saikosaponin-d (SSd) to reduce the damage of kidney in progressive glomerulosclerosis has been demonstrated. In this study, the effects of saikosaponin-d on MC proliferation and synthesis of extracellular matrix proteins were investigated. Rat MCs were isolated from Wistar rats and cultured in Dulbecco's modified Eagle's medium. MCs were challenged with lipopolysacchorides and incubated with different concentrations of SSd. Cell proliferation and cytotoxicity were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and lactate dehydrogenase assays. Type IV collagen, fibronectin, and TGF-beta1 in the conditioned medium were measured. The expression of cyclin-dependent kinase 4, c-Jun, and c-Fos was determined by immunohistochemistry. At a concentration of 4 microg/mL or lower, SSd inhibited MC proliferation but did not cause cell death. SSd also inhibited lipopolysaccharide-induced secretion of type IV collagen, fibronectin, and TGF-beta1 in MCs. Additionally, SSd reduced the expression of CDK4, c-Jun, and c-Fos in MCs. We conclude that SSd inhibited MC proliferation and synthesis of extracullular matrix proteins through the downregulation of the CDK4, c-Jun, and c-Fos genes.
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PMID:Mechanism of saikosaponin-d in the regulation of rat mesangial cell proliferation and synthesis of extracellular matrix proteins. 1753 96

The inhibitory effects of 2,3,5,4'-tetrahydroxystilbene-2-O-beta-d-glucoside (THSG), extracted from the roots of Polygonum multiflorum Thunb, on inflammatory activity in animal models and cyclooxygenase-2 (COX-2) activity in lipopolysaccharide (LPS)-induced mouse RAW264.7 macrophage cells were investigated. The carrageenin (CGN)-induced rat paw oedema model and dimethylbenzene-induced mouse ear oedema model were prepared; MTT assay, semi-quantitative RT-PCR, Western blot and ELISA were adopted. THSG 2.3, 4.6 and 9.2 mg kg(- 1) by oral administration inhibited mouse ear oedema and the percentage of inhibition of THSG 9.2 mg kg(- 1) is 87%. THSG 3.2, 6.4 and 12.8 mg kg(- 1) by oral administration dose-dependently inhibited rat paw oedema and the percentage of inhibition of THSG 12.8 mg kg(- 1) is 56% at 6 h. Indomethacin 13 and 9 mg kg(- 1) showed 90% and 57% inhibition in the same animal models, respectively. LPS 1 microg ml(- 1) significantly up-regulated prostaglandin E(2) (PGE(2)) production (inducing COX-2 activity) by 35% (exogenous arachidonic acid, AA), which was dose-dependently decreased by THSG 1, 10, and 100 micromol L(- 1) and the percentage of inhibition of THSG 10 micromol L(- 1) was 40%. NS-398 10 micromol L(- 1) decreased PGE(2) production by 42%. THSG 1, 10, 100 micromol L(- 1) was shown to markedly inhibit the LPS-induced COX-2 protein and mRNA expression in RAW264.7 cells (P < 0.05) but had no effect on COX-1 protein and mRNA (P>0.05). In summary, the data showed that THSG possessed an anti-inflammatory effect, which was perhaps related to the inhibition of COX-2 enzyme activity and expression in RAW264.7 macrophage cells.
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PMID:Inhibitory effects of 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside on experimental inflammation and cyclooxygenase 2 activity. 1761 21

We investigated the in vitro anti-inflammatory effects of Cinnamaldehyde, a cytokine production inhibitor isolated from an essential oil produced from the leaves of Cinnamomum osmophloeum Kaneh, and its mechanism of action. Although Cinnamaldehyde has been reported to have contact sensitizing properties at high concentration (mM), we found that low concentration of Cinnamaldehyde (muM) inhibited the secretion of interleukin-1beta and tumor necrosis factor alpha within lipopolysaccharide (LPS) or lipoteichoic acid (LTA) stimulated murine J774A.1 macrophages. Cinnamaldehyde also suppressed the production of these cytokines from LPS stimulated human blood monocytes derived primary macrophages and human THP-1 monocytes. Furthermore, Cinnamaldehyde also inhibited the production of prointerleukin-1beta within LPS or LTA stimulated human THP-1 monocytes. Reactive oxygen species release from LPS stimulated J774A.1 macrophages was reduced by Cinnamaldehyde. The phosphorylation of extracellular signal-regulated kinase 1/2 and c-Jun N-terminal kinase 1/2 induced by LPS was also inhibited by Cinnamaldehyde; however, Cinnamaldehyde neither antagonize the binding of LPS to the cells nor alter the cell surface expression of toll-like receptor 4 and CD14. In addition, we also noted that Cinnamaldehyde appeared to elicit no cytotoxic effect upon J774A.1 macrophages under our experimental conditions, although Cinnamaldehyde reduced J774A.1 macrophages proliferation as analysed by MTT assay. Our current results have demonstrated the anti-oxidation and anti-inflammatory properties of Cinnamaldehyde that could provide the possibility for Cinnamaldehyde's future pharmaceutical application in the realm of immuno-modulation.
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PMID:Cinnamaldehyde inhibits pro-inflammatory cytokines secretion from monocytes/macrophages through suppression of intracellular signaling. 1786 67

Most of the available animal antimicrobial peptides (AMPs) have been tested against bacteria and fungi, but very few against protozoan parasites. In the present study, we investigated the antiparasitic activity of different AMPs isolated from aquatic animals: tachyplesin (Tach, from Tachypleus tridentatus), magainin (Mag, from Xenopus laevis), clavanin (Clav, from Styela clava), penaeidin (Pen, from Litopenaeus vannamei), mytilin (Myt, from Mytilus edulis) and anti-lipopolysaccharide factor (ALF, from Penaeus monodon). The antiparasitic activity was evaluated against the promastigote form of Leishmania braziliensis and epi and trypomastigote forms of Trypanosoma cruzi, through the MTT method. Tach was the most potent peptide, killing completely L. braziliensis and trypomastigote T. cruzi from 12.5microM, whereas Pen and Clav were weakly active against trypomastigotes and Myt against L. braziliensis, only at a high concentration (100microM). Tach and Mag were markedly hemolytic at high concentrations, whereas the other peptides caused only a slight hemolysis (<10% up to 50microM). Our results point to Tach as the only potential candidate for further investigation and potential application as a therapeutic agent.
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PMID:Trypanocidal and leishmanicidal activities of different antimicrobial peptides (AMPs) isolated from aquatic animals. 1788 7

Effect of methyl carbonate pesticide, carbonyl, was studied on macrophage functions, lymphocyte proliferation and delayed type hypersensitivity response. Sixteen adult chicken, vaccinated against Newcaslte disease, were procured and randomly divided in two experimental groups. Chicken of group I served as control, while group II birds were given carbaryl at 20 ppm (No observable effect level, NOEL) in feed for 3 months. To measure the functional activity of phagocytic cells, nitroblue tetrazolium (NBT) reduction test was performed on peripheral blood leucocytes. Concanvalin A (Con-A) and lipopolysaccharide stimulated proliferation of T and B lymphocytes was assessed using MTT dye method. At the end of experiment, the phagocytic capacities of macrophages were significantly reduced in carbaryl treated group. Lymphocyte proliferation responses to Con-A and LPS were (23 and 28%, respectively lower) in chicken fed with carbaryl. Delayed hypersensitivity reaction to tuberculin was reduced to 77% of control values indicating inhibition of cell mediated immune response. The present study suggested of immunosuppressive effect of (NOEL dose carbaryl) in chicken.
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PMID:Immunotoxicity of carbaryl in chicken. 1794 37


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