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

Natural products are known to be sources of bioactive components exerting antioxidative and anti-inflammatory activities. We evaluated the suppressive effects of the methanol extract (0-45 microg/mL) of the aerial parts of Saururus chinensis (Lour.) Baill (Saururaceae) on lipopolysaccharide (LPS)-stimulated nitric oxide (NO) production and oxidative stress buildup in the RAW 264.7 murine macrophages. Treatment of RAW 264.7 cells with S. chinensis methanol extract (SME) significantly reduced LPS-stimulated NO production in a concentration-dependent manner. Treatment with SME reduced thiobarbituric acid-reactive substances accumulation and enhanced glutathione levels and activities of antioxidative enzymes, including superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, in LPS-stimulated macrophages compared with LPS-only treated cells. Expression of inducible NO synthase (iNOS) mRNA was also suppressed in SMEtreated cells. The specific DNA binding activities of nuclear factor kappaB (NFkappaB) on nuclear extracts from SME-treated cells were significantly suppressed. These results suggest that SME has antioxidative and anti-inflammatory activities by enhancing antioxidative defense systems and suppressing NO production via the down-regulation of iNOS expression and NFkappaB activity.
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PMID:Antioxidative and anti-inflammatory effects of Saururus chinensis methanol extract in RAW 264.7 macrophages. 1611 11

This study aimed to investigate the effect of sesame oil on oxidative stress-associated renal injury induced by lipopolysaccharide in rats. The effects of sesame oil on renal injury, oxidative stress, hydroxyl radical, superoxide anion, nitric oxide, and proinflammatory cytokines were assessed after a lipopolysaccharide challenge. Sesame oil attenuated lipopolysaccharide-induced renal injury, decreased lipid peroxidation, increased the activities of superoxide dismutase, catalase, and glutathione peroxidase, reduced hydroxyl radical generation and nitric oxide production, and had no effect on superoxide anion generation in lipopolysaccharide-challenged rats. In addition, sesame oil significantly decreased tumor necrosis factor-alpha and interleukin 1beta production 1 and 6 h, respectively, after lipopolysaccharide administration in mice. Thus, sesame oil attenuates oxidative stress-associated renal injury via reduction of the production of nitric oxide and the generation of proinflammatory cytokines in endotoxemic rats.
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PMID:Effect of sesame oil on oxidative-stress-associated renal injury in endotoxemic rats: involvement of nitric oxide and proinflammatory cytokines. 1652 61

Microbial infections, localized as well as systemic, are known to cause transitive or permanent male infertility. However, the mechanisms of infection-induced infertility are largely unknown. Earlier reports showed that steroidogenesis and spermatogenesis are affected during bacterial lipopolysaccharide (LPS)-induced acute inflammation. The present study used an LPS rat model to investigate the role of oxidative stress in spermatogenesis. Intraperitoneal administration of bacterial LPS (5mg/kg body weight) to adult male albino rats elevated testicular malondialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE), and decreased the activities of testicular antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase, and glutathione reductase. The GSH/GSSG ratio also decreased significantly. Time series analysis revealed transitory oxidative stress and expression of inflammatory mediators such as interleukin-1beta (IL-1beta), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) from 3h to 12h after LPS. Testicular expression of steroidogenic acute regulatory (StAR) protein decreased to 24h, in correlation with damage to spermatogenesis. These data are consistent with oxidative stress as a major causal factor in altered steroidogenesis, spermatogenesis, and perhaps male infertility during endotoxin-induced acute inflammation.
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PMID:Bacterial lipopolysaccharide-induced oxidative stress in the impairment of steroidogenesis and spermatogenesis in rats. 1664 80

Liver genes related to phase I and phase II detoxification, as well as inhibition of reactive oxygen species (ROS) production, were cloned, and their response to microcystin-LR (MC-LR) and lipopolysaccharide (LPS) exposure via intraperitoneal injection, was determined in a phytoplanktivorous fish, Nile tilapia (Oreochromis niloticus). The cloned full-length cDNA of tilapia soluble glutathione S-transferase (sGST) was classified as alpha-class GST based on their amino acid sequence identity with other species. The tilapia sGST clone was 861 bp in length, and contained a 25 bp 5'-UTR, a 167 bp 3'-UTR and an open reading frame of 669 bp, encoding a polypeptide of 222 amino acids. Using genome walker method, a 366 bp 5'-flanking sequence of tilapia sGST gene was further obtained, and the possible regulatory elements were identified. Partial cDNA sequences of glutathione peroxidase (GPX) and uncoupling protein 2 (UCP2) were also obtained by PCR using degenerate primers from tilapia liver. To study the transcriptional response of liver genes to microcystin treatment, tilapia were respectively exposed to a single 50 microg kg(-1) body weight (bwt) dose of pure MC-LR, a single 2 mg kg(-1) bwt dose of LPS and a co-exposure MC-LR and LPS (50 microg kg(-1) bwt+2 mg kg(-1) bwt), and were then sacrificed at 24 h post-exposure. Using beta-actin as external control, a significant increase (about 80%) in sGST mRNA expression was found in response to the MC-LR exposure after 24 h (P < 0.05), indicating the importance of sGST in microcystin detoxification. A slight decrease of sGST mRNA expression was observed in the liver of tilapia, exposed to LPS and MC-LR+LPS. It seems that the LPS response element (LPSRE), identified in the promoter region of tilapia sGST gene, may be functional at a rather low level. In contrast, the levels of cytochrome P450 1A (CYP1A) mRNA expression were found to keep unchanged to either MC-LR, or LPS, or MC-LR+LPS treatment, indicating that unlike the phase II enzyme (sGST), the phase I enzyme (CYP1A) might not play an important role in the detoxification process of microcystins. Although not significant, the mRNA expression level of GPX tended to increase in the liver of tilapia exposed to both MC-LR and LPS (P > 0.05). In addition, a significant increase in UCP2 mRNA expression was observed in the liver of tilapia exposed to LPS (P < 0.05), as well as an obvious but not significant increase in MC-LR exposure group. We suggest that phase II detoxification enzyme, instead of phase I detoxification enzyme, might be responsible for the strong tolerance of the phytoplanktivorous fish to microcystins, and hepatocyte proteins coping with oxidative stress (GPX and UCP2), might also have some auxiliary effect. In addition, the rather low and insignificant response of tilapia sGST gene to the inhibitory effect of LPS exposure, might possibly be critical to the phytoplanktivorous fish to utilize toxic blue-green algae.
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PMID:Structural and functional characterization of microcystin detoxification-related liver genes in a phytoplanktivorous fish, Nile tilapia (Oreochromis niloticus). 1704 49

Nitric oxide is known to modulate intracellular glutathione levels, but the relationship between nitric oxide synthesis and glutathione metabolism during endotoxemia is unknown. The present study was designed to examine the effects of increased nitric oxide formation on hepatic glutathione synthesis and antioxidant defense in endotoxemic mice. Our results demonstrate that hepatic glutathione synthesis is decreased for 24 h following injection of lipopolysaccharide (LPS). Administration of the cysteine precursor, L-2-oxothiazolidine-4-carboxylic acid (OTZ), failed to normalize hepatic glutathione concentration, and suggests that decreased gamma-glutamylcysteine ligase activity is primarily responsible for the decrease in hepatic glutathione levels during endotoxemia. Inhibition of nitric oxide synthesis prevented the endotoxin-induced changes in hepatic and plasma glutathione status and up-regulated liver glutathione and cysteine synthesis pathways at the level of gene expression. Furthermore, whereas the activity of glutathione peroxidase and glutathione S-transferase decreased during endotoxemia, both of these changes were prevented by inhibition of nitric oxide synthesis. In conclusion, increased nitric oxide synthesis during endotoxemia causes marked changes in glutathione flux and defenses against oxidative stress in the liver.
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PMID:Nitric oxide modulates glutathione synthesis during endotoxemia. 1715 84

The effect of experimental burn trauma (20%) on myeloperoxidase (MPO) and antioxidant enzymes (catalase, glutathione peroxidase (GPO), glutathione-S-transferase (GST)) was studied in unburned skin, epidermis (20 mm from the burned area) and the wound tissue of rats. The most common features were the increase of MPO on the 1st day and a delayed increase of GPO and GST after the 4th day. The additional operations (necrectomy) and lipopolysaccharide administration induced marked inflammatory reaction in skin and epidermis (evaluated by the increase in MPO and GPO/GST activities).
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PMID:[Antioxidant enzymes in skin experimental burn trauma]. 1728 49

We previously reported that injection of bacterial lipopolysaccharide (LPS) into gravid female rats at embryonic day 10.5 resulted in a birth of offspring with fewer than normal dopamine (DA) neurons along with innate immunity dysfunction and many characteristics seen in Parkinson's disease (PD) patients. The LPS-exposed animals were also more susceptible to secondary toxin exposure as indicated by an accelerated DA neuron loss. Glutathione (GSH) is an important antioxidant in the brain. A disturbance in glutathione homeostasis has been proposed for the pathogenesis of PD. In this study, animals prenatally exposed to LPS were studied along with an acute intranigral LPS injection model for the status of glutathione homeostasis, lipid peroxidation, and related enzyme activities. Both prenatal LPS exposure and acute LPS injection produced a significant GSH reduction and increase in oxidized GSH (GSSG) and lipid peroxide (LPO) production. Activity of gamma-glutamylcysteine synthetase (GCS), the rate-limiting enzyme in de novo GSH synthesis, was up-regulated in acute supranigral LPS model but was reduced in the prenatal LPS model. The GCS light subunit protein expression was also down-regulated in prenatal LPS model. GSH redox recycling enzyme activities (glutathione peroxidase, GPx and glutathione reducdase, GR) and glutathione-S-transferase (GST), gamma-glutamyl transpeptidase (gamma-GT) activities were all increased in prenatal LPS model. Prenatal LPS exposure and aging synergized in GSH level and GSH-related enzyme activities except for those (GR, GST, and gamma-GT) with significant regional variations. Additionally, prenatal LPS exposure produced a reduction of DA neuron count in the substantia nigra (SN). These results suggest that prenatal LPS exposure may cause glutathione homeostasis disturbance in offspring brain and render DA neurons susceptible to the secondary neurotoxin insult.
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PMID:Altered glutathione homeostasis in animals prenatally exposed to lipopolysaccharide. 1729 29

Intraperitoneal injection of bacterial lipopolysaccharide in a dose of 1 mg/kg was followed by prestimulation of whole blood leukocytes in rats. Activities of peroxide- and lipoperoxide-utilizing antioxidant enzymes glutathione peroxidase, glutathione S-transferase, and catalase increased 1 day after lipopolysaccharide administration, while the content of malonic dialdehyde in the skin remained unchanged.
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PMID:Effect of endotoxemia on skin antioxidant enzymes under experimental conditions. 1741 24

D-Galactosamine (GalN) depletes UTP primarily in liver, resulting in decreased RNA synthesis in hepatocytes. When given together with a sublethal dose of lipopolysaccharide (LPS), GalN highly sensitizes animals to produce apoptotic liver injury with severe hepatic congestion, resulting in rapid death. Melatonin is a cytokine modulator, antioxidant and anti-apoptotic agent. In the present study, we investigated the effect of melatonin on LPS-induced apoptotic liver damage in GalN-sensitized mice. Female CD-1 mice were intraperitoneally (i.p.) injected with melatonin (5.0mg/kg) 30min before GalN/LPS (700mg10microg/kg, i.p.), another two doses of melatonin (2.5mg/kg, i.p.) being administered 1 and 2h after GalN/LPS. Results showed that serum alanine aminotransferase (ALT) activities were markedly increased 8h after GalN/LPS treatment, massive hemorrhage being observed in histological sections of liver from GalN/LPS-treated mice. Melatonin significantly attenuated GalN/LPS-induced elevation of serum ALT. In parallel, melatonin distinctly improved GalN/LPS-induced congestion. Additional experiment showed that melatonin significantly attenuated GalN/LPS-induced hepatic apoptosis, measured by inhibition of caspase-3 activities and attenuation of DNA laddering. Furthermore, melatonin markedly increased hepatic Se-dependent glutathione peroxidase (GSH-Px) and glutathione reductase (GSH-Rd) activities and attenuated hepatic glutathione (GSH) depletion in GalN/LPS-treated mice. Increases in serum tumor necrosis factor alpha (TNF-alpha), which were observed in GalN/LPS-treated mice, were significantly reduced by melatonin. However, melatonin had no effect on LPS-evoked nitric oxide production in GalN-sensitized mice. Taken together, these results indicate that melatonin protected against LPS-induced liver damage in GalN-sensitized mice through its strong ROS-scavenging, antiinflammatory and antiapoptotic effects.
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PMID:Melatonin attenuates lipopolysaccharide (LPS)-induced apoptotic liver damage in D-galactosamine-sensitized mice. 1760 19

1. The influence of dietary conjugated linoleic acid (CLA) on the antioxidant status in the absence or presence of endotoxin exposure was studied with male broiler chicks. 2. In experiment 1, a total of 240 1-d-old broilers were allotted into 4 dietary groups (0, 2.5, 5.0 or 10.0 g pure CLA/kg) to study the influence of CLA on growth performance and antioxidant defence systems. The results showed that growth performance was not altered by 42 d of CLA consumption. Increased total superoxide dismutase (TSOD) activities in liver, serum and muscle were observed in chicks given 10.0 g CLA/kg diet. Dietary CLA at 10.0 g/kg also markedly elevated liver catalase (CAT) activity. Malondialdehyde (MDA), a marker of lipid peroxidation, decreased in liver, serum and muscle in chicks given 5.0 and 10.0 g CLA/kg diet. 3. In experiment 2, a total of 120 1-d-old broilers were fed on a control diet (without CLA) or 10.0 g CLA/kg diet. Half of the birds fed on each diet were injected intraperitoneally with 0.25 mg/kg body weight of Salmonella enteritidis lipopolysaccharide (LPS) at 16, 18 and 20 d of age. Decreased glutathione peroxidase (GSH-Px), TSOD activity and increased ceruloplasmin and MDA concentrations were seen in the challenged chicks. Dietary CLA prevented the loss of body weight gain and feed conversion ratio of chicks followed repeated endotoxin exposure. CLA partially inhibited the increase of serum ceruloplasmin and MDA at 17 and 21 d of age and notably suppressed the decrease of serum TSOD activity at 21 d of age. 4. These results suggested that dietary CLA enhances the activity of antioxidant enzymes including TSOD and CAT. Supplementation of CLA has been shown to ameliorate the antioxidant balance and performance of chicks during oxidative stress.
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PMID:Dietary conjugated linoleic acid improves antioxidant capacity in broiler chicks. 1840 96


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