Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.11.1.6 (catalase)
 55,569 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the present study was to evaluate the possibility to modulate the early inflammatory response in vitro by coating titanium surfaces with candidate proinflammatory (fibrinogen coated turned titanium "Fib") and antiinflammatory proteins (catalase on top of fibrinogen coated turned titanium "Cat"). Additionally, turned titanium surfaces (Ti) were used as controls. The discs were incubated with human mononuclear cells. Adhered cells were investigated with respect to number, viability, differentiation (acute marker 27E10 vs. chronic marker RM3/1), and cytokine production (TNF-alpha and IL-10), after 24 and 72 h. The results indicated that it is possible to modulate the inflammatory response with protein coatings. However, the strongest inflammatory response, indicated by increased number of adhered cells and release of pro and antiinflammatory mediators, was induced by Cat. Furthermore, the cytokine production on this surface was not sensitive to LPS stimulation. Differentiation measured as the expression of the chronic cell surface marker, dominated after 72 h for all surface modifications and Cat displayed an increased number compared to the others. A decrease in the total number of adhered cells and amounts of TNF-alpha were observed on all surfaces over time. The cell viability was, in general, high for all tested surfaces. In conclusion, the study proved it possible to influence the early inflammatory response in vitro by immobilizing protein coatings to titanium surfaces. However, the catalase surface demonstrated the strongest inflammatory response, and the possibility to selectively use the potent antiinflammatory capacity of catalase needs to be further evaluated.
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PMID:Inflammatory response to titanium surfaces with fibrinogen and catalase coatings: an in vitro study. 1712 Feb 11

In vivo protective and alleviative effects of s-allyl cysteine (SAC), s-ethyl cysteine (SEC), s-methyl cysteine (SMC), and s-propyl cysteine (SPC) against alcohol-induced hepatotoxicity in Balb/cA mice were studied. In the preventive study, SAC, SEC, SMC, or SPC, each agent at 1 g/L, was added into the drinking water for 3 wk, and the mice were then treated with ethanol to induce acute liver injury. In the alleviative study, mice were first treated by ethanol followed by the 4 agent treatments for 3 wk. The preintake of these agents significantly attenuated subsequent alcohol-induced lipid oxidation, glutathione (GSH) depletion, and activity reduction of catalase and glutathione peroxidase (P < 0.05); also attenuated were the alcohol-induced elevation of c-reactive protein (CRP), interleukin-6 (IL-6), IL-10 and tumor necrosis factor (TNF)-alpha (P < 0.05). The preintake of these agents also significantly retarded alcohol-induced cytochrome P450 2E1 (CYP2E1) activity increase (P < 0.05). In the alleviative study, posttreatments from the 4 agents restored liver GSH content (P < 0.05); however, only SEC and SPC posttreatments significantly reduced lipid oxidation and alleviated the alcohol-induced elevation of CRP, IL-6, IL-10, and TNF-alpha (P < 0.05). SEC and SPC posttreatments also significantly diminished alcohol induced CYP2E1 activity (P < 0.05). These results support that SEC and SPC could provide both preventive and alleviative effects against alcohol-induced hepatotoxicity through suppression of oxidation and inflammation.
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PMID:Protective and alleviative effects from 4 cysteine-containing compounds on ethanol-induced acute liver injury through suppression of oxidation and inflammation. 1799 65

Diabetic patients reveal significant disorders, such as nephropathy, cardiomyopathy, and neuropathy. As oxidative stress and inflammation seem to be implicated in the pathogenesis of diabetic brain, we aimed to investigate the effects of caffeic acid phenethyl ester (CAPE) on oxidative stress and inflammation in diabetic rat brain. Diabetes was induced by a single dose of streptozotocin (45 mg kg(-1), i.p.) injection into rats. Two days after streptozotocin treatment 10 microM kg(-1) day(-1) CAPE was administrated and continued for 60 days. Here, we demonstrate that CAPE significantly decreased the levels of nitric oxide and malondialdehyde induced by diabetes, and the activities of catalase, glutathione peroxidase, and xanthine oxidase in the brain. However, glutathione levels were increased by CAPE. The mRNA expressions of tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma, and inducible nitric oxide synthase (iNOS) were remarkably enhanced in brain by diabetes. CAPE treatments significantly suppressed these inflammatory cytokines (about 70% for TNF-alpha, 26% for IFN-gamma) and NOS (completely). Anti-inflammatory cytokine IL-10 mRNA expression was not affected by either diabetes or CAPE treatments. In conclusion, diabetes induces oxidative stress and inflammation in the brain, and these may be contributory mechanisms involved in this disorder. CAPE treatment may reverse the diabetic-induced oxidative stress in rat brains. Moreover, CAPE reduces the mRNA expressions of TNF-alpha and IFN-gamma in diabetic brain; suggesting CAPE suppresses inflammation as well as oxidative stress occurred in the brain of diabetic patients.
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PMID:Caffeic acid phenethyl ester (CAPE) protects brain against oxidative stress and inflammation induced by diabetes in rats. 1826 48

The endocrine and immune systems modulate ovarian function. The aim of the present work was to compare the status of various modulating factors in two well-defined stages of corpus luteum (CL) development (the functional stage and the regressing stage) by means of a gonadotropin-synchronised mouse model. At the regressing stage of CL development, we found that ovarian tissue showed increased prostaglandin (PG) F(2alpha) and diminished PGE levels concomitantly with enhanced protein abundance of ovarian cyclooxygenase 2, the inducible isoform of the limiting enzyme of PG synthesis. We also found both enhanced lipid peroxidation and enhanced total superoxide dismutase activity, as well as inhibited catalase activity and inhibited total hydroxyl radical scavenger capacity, when compared with ovaries at the functional stage. In addition, at the regressing stage we observed an increased percentage of CD8+ (cytotoxic/suppressor) T-cells and a decreased percentage of CD4+ (helper) T-cells from ovarian-draining lymph nodes. Also, the serum interleukin (IL)-2, IL-4 and IL-10 were diminished as compared with the functional stage. We conclude that a pro-oxidant status together with a pro-inflammatory response is responsible for the loss of luteal function.
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PMID:Regulation of functional and regressing stages of corpus luteum development in mice. Role of reactive oxygen species. 1884 78

This study was designed to compare the effect of pretreatment with N-acetylcysteine (NAC) and beta -glucan (beta GLU) on inflammatory response in a rat model of sepsis. The study was performed in the animal laboratory of the Kahramanmaras Sutcu Imam University, School of Medicine. Forty rats were randomized into four groups (control, sham, NAC, and beta GLU). Control and Sham groups received saline or NAC (200 mg/kg, po) in the NAC group and beta GLU (50 mg/kg, po) in the betaGLU group via intragastric gavage once a day for 10 days and 30 min prior to surgery. Sepsis was induced by cecal ligation and puncture (CLP) in rats. In the NAC, beta GLU, and control groups, a laparotomy was performed with the CLP procedure. In the sham group, laparotomy was performed and cecum was manipulated but not ligated or perforated. TNF-alpha and IL-6 levels were significantly elevated in the control group and decreased in the NAC and beta GLU groups. IL-10 levels were significantly increased in the beta GLU group (p < .05). Superoxide dismutase and catalase levels in the liver tissue were significantly increased in the NAC and beta GLU groups, whereas superoxide dismutase levels were higher in the beta GLU pretreatment group than the NAC pretreatment group (p < 0.05). Malondialdehyde levels in the liver tissue were significantly elevated in the control group and decreased in the NAC and beta GLU groups (p < .05). Prophylactic administration of NAC or beta GLU similarly ameliorated sepsis syndrome by reduction of the proinflammatory cytokines and increase of the anti-inflammatory cytokine levels and accession of cellular antioxidants, which protect cells from oxidative stress, thereby recruiting inflammatory cells into tissue.
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PMID:Protective effects of N-acetylcysteine and beta-glucan pretreatment on oxidative stress in cecal ligation and puncture model of sepsis. 1916 Jan 31

Curcumin is a polyphenol derived from the dietary spice turmeric. It has been shown to regulate numerous transcription factors, cytokines, adhesion molecules, and enzymes that have been linked to inflammation. In addition to inhibiting the growth of a variety of pathogens, curcumin has been shown to have nematocidal activity. The present study was designed to evaluate the schistosomicidal activity of curcumin in vivo as well as immunomodulation of granulomatous inflammation and liver pathology in acute schistosomiasis mansoni. Mice were infected each with 80 Schistosoma (S.) mansoni cercariae and injected intraperitoneally with curcumin at a total dose of 400mg/kg body weight. Curcumin was effective in reducing worm and tissue-egg burdens, hepatic granuloma volume and liver collagen content by 44.4%, 30.9%, 79%, and 38.6%, respectively. Curcumin treatment restored hepatic enzymes activities to the normal levels and enhanced catalase activity in the liver tissue of infected mice. Moreover, hepato-spleenomegaly and eosinophilia induced by S. mansoni infection were largely improved with curcumin treatment. Infected mice treated with curcumin showed low serum level of both interleukin (IL)-12 and tumor necrosis factor alpha (TNF-alpha), but IL-10 level was not significantly altered. Specific IgG and IgG1 responses against both soluble worm antigen (SWAP) and soluble egg antigen (SEA) were augmented with curcumin treatment, but IgM and IgG2a responses were not significantly changed. In conclusion, curcumin treatment modulates cellular and humoral immune responses of infected mice and lead to a significant reduction of parasite burden and liver pathology in acute murine schistosomiasis mansoni.
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PMID:Immunomodulatory effects of curcumin treatment on murine schistosomiasis mansoni. 1924 23

Alcohol consumption is implicated in the genesis of a spectrum of liver abnormalities, which are associated with a number of factors. In the present study, time-dependent effects of ethanol on cytokines (TNF-alpha, IL-2, IL-4, IL-10, IFN-gamma, VEGF-A and TGF-beta1) in serum, and blood oxidative stress parameters such as reduced glutathione content, TBARS level and activities of GPx, GR, GST, catalase and SOD in 8-10 weeks-old male BALB/c mice have been investigated. Ethanol administered @ 1.6 g/kg body wt/day significantly increased the activities of liver marker enzymes AST, ALT and ALP. Serum nitrite levels and haemolysate TBARS level also increased, while total antioxidant status in serum and GSH content in whole blood hemolysate decreased from 4th week onwards of exposure. In spite of the increased serum nitrite level and GST activity in the haemolysate, albumin level in serum, GPx and GR activities in haemolysate decreased after 12 weeks of exposure. Chronic ethanol treatment did not show any effect on IL-2, but IL-4 level was reduced and other cytokines such as IL-10, TNF-alpha, IFN-gamma, TGF-beta1 and VEGF-A levels were increased significantly after 12 weeks. The study indicates a relationship between free radical generation and immune response, and suggests that ethanol-induced liver damage is associated with oxidative stress and immunological alterations in a time-dependent manner.
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PMID:Time-dependent effects of ethanol on blood oxidative stress parameters and cytokines. 1937 64

Sepsis/multiple organ dysfunction syndrome (MODS) is a major cause of high mortality in the intensive care unit. We have recently reported that 100% oxygen treatment is beneficial to mice with zymosan-induced sterile inflammation by increasing antioxidant enzymatic activities. Yet, the use of hyperoxia is hindered by concerns that it could exacerbate organ injury by increasing free radical formation. It is believed that systemic inflammation and overproduction of reactive oxygen species (ROS) contribute to the mechanism underlying sepsis/MODS. A ROS scavenger has been proven to protect against sepsis/MODS in some animal models. Therefore, we hypothesized that ROS scavenger pretreatment might enhance the protective action of 100% oxygen treatment against zymosan-induced sterile inflammation in mice. In the present study, we showed that 100% oxygen treatment prevented the abnormal changes in serum biochemical parameters, tissue oxygenation, and organ histopathology, and improved the 14-day survival rate in zymosan-stimulated mice, indicating that 100% oxygen treatment had a protective action on sterile inflammation. We found that pretreatment with a ROS scavenger (N-acetylcysteine, vitamin C, or dimethylthiourea) abolished this protective action of 100% oxygen treatment. We also showed that 100% oxygen treatment decreased the levels of serum proinflammatory cytokines (TNF-alpha, IL-6, and high-mobility group box 1), increased the level of serum anti-inflammatory cytokine (IL-10), and upregulated the activities of serum and tissue antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) in zymosan-stimulated mice, which were reversed by the pretreatment with a ROS scavenger (N-acetylcysteine, vitamin C, or dimethylthiourea). We thus conclude that ROS scavenger pretreatment partly abolishes the protective effects of 100% oxygen treatment on sterile inflammation in mice by regulating inflammatory cytokines as well as antioxidant enzymes.
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PMID:Effects of reactive oxygen species scavenger on the protective action of 100% oxygen treatment against sterile inflammation in mice. 1978 62

Protective effects of carnosine or histidine against acetaminophen-induced hepatotoxicity in Balb/cA mice were examined. Each compound, at 0.5, 1, or 2 g/L, was added into the drinking water for 4 wk. Acute liver injury was induced by acetaminophen treatment intraperitoneally (i.p. 350 mg/kg body weight). Acetaminophen treatment significantly depleted hepatic GSH and ascorbic acid levels, increased hepatic level of malonyldialdehyde (MDA), reactive oxygen species (ROS), and oxidized glutathione (GSSG), as well as decreased hepatic activity of glutathione peroxidase (GPX), catalase, and superoxide dismutase (SOD) (P < 0.05). However, the pre-intake of carnosine or histidine significantly alleviated acetaminophen-induced oxidative stress by increasing GSH content, decreasing MDA, ROS, and GSSG formations, and retaining activity of GPX, catalase, and SOD in liver (P < 0.05). The pre-intake of these compounds also significantly retarded subsequent acetaminophen-induced increase of cytochrome P450 2E1 activity (P < 0.05). Acetaminophen treatment increased the hepatic levels of interleukin (IL)-6, IL-10, tumor necrosis factor (TNF)-alpha, and monocyte chemoattractant protein (MCP)-1 (P < 0.05). The pre-intake of carnosine or histidine significantly diminished acetaminophen-induced elevation of these cytokines (P < 0.05). The impact of these compounds on mRNA expression of GPX, TNF-alpha, and MCP-1 indicated that these compounds could act at a transcription level. These results support that carnosine and histidine are potent hepatoprotective agents.
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PMID:Protective effects from carnosine and histidine on acetaminophen-induced liver injury. 1979 68

The aim of this paper is to study the myocardial damage secondary to long-term streptozotocin-induced type 1 diabetes mellitus (DM1). Normotensive and spontaneously hypertensive rats (SHR) received either streptozotocin injections or vehicle. After 22 or 6 wk, DM1, SHR, DM1/SHR, and control rats were killed, and the left ventricles studied by histology, quantitative PCR, Western blot, ELISA, and electromobility shift assay. Cardiomyocyte cultures were also performed. The expression of profibrotic factors, transforming growth factor-beta (TGF-beta1), connective tissue growth factor, and matrix proteins was increased, and the TGF-beta1-linked transcription factors phospho-Smad3/4 and activator protein-1 were activated in the DM1 myocardium. Proapoptotic molecules FasL, Fas, Bax, and cleaved caspase-3 were also augmented. Myocardial injury in long-term hypertension shared these features. In addition, hypertension was associated with activation of NF-kappaB, increased inflammatory cell infiltrate, and expression of the mediators [interleukin-1beta (IL-1beta), tumor necrosis factor-alpha, monocyte chemoattractant protein 1, vascular cell adhesion molecule 1, angiotensinogen, and oxidants], which were absent in long-term DM1. At this stage, the combination of DM1 and hypertension resulted in nonsignificant additive effects. Moreover, the coexistence of DM1 blunted the inflammatory response to hypertension. Anti-inflammatory IL-10 and antioxidants were induced in long-term DM1 and DM1/SHR hearts. Myocardial inflammation was, however, observed in the short-term model. In cultured cardiomyocytes, IL-10, TGF-beta1, and catalase blocked the glucose-stimulated expression of proinflammatory genes. Fibrosis and apoptosis are features of long-term myocardial damage in experimental DM1. Associated hypertension does not induce additional changes. Myocardial inflammation is present in hypertension and short-term DM1, but is not a key feature in long-term DM1. Local reduction of proinflammatory factors and expression of anti-inflammatory and antioxidant molecules may underlie this effect.
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PMID:Myocardial fibrosis and apoptosis, but not inflammation, are present in long-term experimental diabetes. 1982 Jan 99


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