Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P05231 (interleukin-6)
 23,907 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Nickel is a metal widely employed in dental alloys, and due to peculiar properties of certain nickel-based materials, it cannot be substituted with other metals in some applications. The release of nickel ions from dental alloys placed into long-term contact with mouth soft tissues is alarming because of the toxic, immunological and carcinogenic effects which have been well documented for some nickel compounds. Our study was focussed on the toxic effects induced "in vitro" on human oral epithelium by the exposure to low concentrations of nickel chloride. In view of this, we adopted a three-dimensional model of epithelial cultures, reconstituted from TR 146 cells, resembling the physiological environment of the oral cavity and useful for biocompatibility testing. The effects on cell viability, apoptosis, cellular content of reduced and oxidized glutathione (GSH and GSSG) and release of prostaglandin E(2) (PGE(2)), interleukin-8 (IL-8) and interleukin-6 (IL-6) were investigated following topical application of a NiCl(2) solution ranging from 7.6mM to 0.05 mM for 72 h. Our findings show that nickel concentrations, which do not significantly modify cell viability and inflammation mediator release, can affect the redox equilibrium and stimulate apoptosis in oral epithelium cells. Further studies are needed to demonstrate the hypothesis that the oxidative imbalance induced by nickel might be implicated in the induction of apoptosis.
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PMID:Toxic effect of nickel in an in vitro model of human oral epithelium. 1601 80

The present study is aimed at investigating the effect of curcumin (CMN) in salvaging endotoxin-induced hepatic dysfunction and oxidative stress in the liver of rodents. Hepatotoxicity was induced by administering lipopolysaccharide (LPS) in a single dose of 1 mg/kg intraperitoneally to the animals, which were being treated with CMN daily for 7 days. Liver enzymes serum alanine aminotransferase (ALT), serum aspartate aminotransferase (AST) and alkaline phosphatase (ALP), total bilirubin and total protein were estimated in serum. Oxidative stress in liver tissue homogenates was estimated by measuring thiobarbituric acid reactive substances (TBARS), glutathione (GSH) content and superoxide dismutase (SOD) activity. Serum and tissue nitrite was estimated using Greiss reagent and served as an indicator of NO production. A separate set of experiments was performed to estimate the effect of CMN on cytokine levels in mouse serum after LPS challenge. LPS induced a marked hepatic dysfunction evident by rise in serum levels of ALT, AST, ALP and total bilirubin (P < 0.05). TBARS levels were significantly increased, whereas GSH and SOD levels decreased in the liver homogenates of LPS-challenged rats. CMN administration attenuated these effects of LPS successfully. Further CMN treatment also regressed various structural changes induced by LPS in the livers of rats and decreased the levels of tumour necrosis factor-alpha and interleukin-6 in mouse plasma. In conclusion, these findings suggest that CMN attenuates LPS-induced hepatotoxicity possibly by preventing cytotoxic effects of NO, oxygen free radicals and cytokines.
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PMID:Inhibition of oxidative stress and cytokine activity by curcumin in amelioration of endotoxin-induced experimental hepatoxicity in rodents. 1687 52

We investigated the protective role of aminoguanidine (AG) in rat liver injury induced by chronic biliary obstruction. Secondary biliary cirrhosis was induced by bile duct ligation for 14 days. Swiss albino rats were divided into three groups: Common bile duct ligated (CBDL) rats; Group A, CBDL rats treated with AG as Group B and simple laparotomy group known as the Sham group; Group C. Group B received 200 mg/kg of AG intraperitoneally daily throughout 14 days. The present data showed decreased gama glutamyl transferase (GGT), aspartate aminotransferase (AST), bilirubin and alanine aminotransferase (ALT) levels in the AG treated rats, when compared with CBDL rats (p < 0.05). In the AG treated rats, tissue levels of malondialdehyde (MDA) were significantly lower than that in CBDL rats (p < 0.001). Although the levels of glutathione (GSH) in AG treated rats were higher and myeloperoxidase (MPO) were lower than that in CBDL rats, the difference was not statistically significant (p > 0.05). The levels of interleukin-1alpha (IL-1alpha) and tumor necrosis factor-alpha (TNF-alpha) were significantly lower and although the levels of interleukin-6 (IL-6) were lower in AG treated rats than that in CBDL rats, the difference was not statistically significant. Administration of AG in the rats with biliary obstruction resulted in inhibition of ductular proliferation and portal inflammation. The present study demonstrates that intraperitoneal administration of AG in CBDL rats maintains antioxidant defenses, reduces liver oxidative and cytokine damage and ductular proliferation and portal inflammation. This effect of AG may be useful in the preservation of liver injury in cholestasis.
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PMID:The effect of aminoguanidine against cholestatic liver injury in rats. 1689 51

The present study was performed to determine whether melatonin protects mouse liver against severe damage induced by acetaminophen (APAP) administration and where melatonin primarily functions in the metabolic pathway of APAP to protect mouse liver against APAP-induced injury. Treatment of mice with melatonin (50 or 100 mg/kg, p.o.) 8 or 4 hr before APAP administration (750 mg/kg, p.o.) suppressed the increase in plasma alanine aminotransferase and aspartate aminotransferase activities in a dose- and a time-dependent manner. Melatonin treatment (100 mg/kg, p.o.) 4 hr before APAP administration remarkably inhibited centrilobular hepatic necrosis with inflammatory cell infiltration and increases in hepatic lipid peroxidation and myeloperoxidase activity, an index of tissue neutrophil infiltration, as well as release of nitric oxide and interleukin-6 into blood circulation at 9 hr after APAP administration. However, melatonin neither affected hepatic reduced glutathione (GSH) content nor spared hepatic GSH consumption by APAP treatment. Moreover, pretreatment with melatonin 4 hr before APAP administration did not influence the induction of hepatic heat shock protein 70 (HSP70) by APAP and melatonin alone did not induce HSP70 in mouse liver. These results indicate that exogenously administered melatonin exhibits a potent hepatoprotective effect against APAP-induced hepatic damage probably downstream of the activity of cytochrome P450 2E1, which works upstream of GSH conjugation in the pathway of APAP metabolism, via its anti-nitrosative and anti-inflammatory activities in addition to its antioxidant activity.
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PMID:Mechanisms of protection by melatonin against acetaminophen-induced liver injury in mice. 1694 81

Curcumin, an anti-inflammatory and antioxidant compound, was evaluated for its ability to suppress acute carbon tetrachloride-induced liver damage. Acute hepatotoxicity was induced by oral administration of CCl4 (4 g/kg, p.o.). Curcumin treatment (200 mg/kg, p.o.) was given before and 2 h after CCl4 administration. Indicators of necrosis (alanine aminotransferase) and cholestasis (gamma-glutamyl transpeptidase and bilirubins) resulted in significant increases after CCl4 intoxication, but these effects were prevented by curcumin treatment. As an indicator of oxidative stress, GSH was oxidized and the GSH/GSSG ratio decreased significantly by CCl4, but was preserved within normal values by curcumin. In addition to its antioxidants properties, curcumin is capable of preventing NF-kappaB activation and therefore to prevent the secretion of proinflammatory cytokines. Therefore, in this study we determined the concentrations of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and interleukin-6 (IL-6) mRNA, and NF-kappaB activation. CCl4-administered rats depicted significant increases in TNF-alpha, IL-1beta, and IL-6 production, while curcumin remarkably suppressed these mediators of inflammation in liver damage. These results were confirmed by measuring TNF-alpha, and IL-1beta protein production using Western Blot analysis. Accordingly, these proteins were increased by CCl4 and this effect was abolished by curcumin. Administration of CCl4 induced the translocation of NF-kappaB to the nucleus; CCl4 induced NF-kappaB DNA binding activity was blocked by curcumin treatment. These findings suggest that curcumin prevents acute liver damage by at least two mechanisms: acting as an antioxidant and by inhibiting NF-kappaB activation and thus production of proinflammatory cytokines.
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PMID:Curcumin protects against acute liver damage in the rat by inhibiting NF-kappaB, proinflammatory cytokines production and oxidative stress. 1738 25

Zinc (Zn) has been reported to influence the susceptibility of the host to a diverse range of infectious pathogens, including viruses, bacteria, fungi and protozoa. We report here an evaluation of the effects of Zn supplementation on Salmonella enterica serovar Typhimurium (S. typhimurium)-induced hepatic injury in the murine model. Zinc levels in the plasma and liver tissues were measured by atomic absorption spectroscopy. The effect of Zn supplementation was evaluated by assessing the bacterial load and levels of lipid peroxidation (LPO), antioxidants and monokines present in the hepatic tissue as well as by histopathological studies. Zinc supplementation reduced the bacterial load in the liver and reversed hepatic microscopic abnormalities. It also decreased the levels of LPO but increased the levels of reduced glutathione (GSH) as well as the activities of superoxide-dismutase (SOD) and catalase in the livers of infected mice supplemented with Zn compared to the livers of infected mice not supplemented with Zn. Zinc supplementation was also able to modulate the levels of monokines such as tumour necrosis factor alpha (TNF-alpha), interleukin-1 (IL-1) and interleukin-6 (IL-6). Our results indicate a role for Zn in downregulating oxidative stress and upregulating antioxidant defense enzymes through the action of monokines, suggesting that supplementation with Zn has a protective function in Salmonella-induced liver injury.
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PMID:Amelioratory effects of zinc supplementation on Salmonella-induced hepatic damage in the murine model. 1793 36

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

The purposes of this study were to investigate the effects of strenuous exercise on apoptosis of the gastrocnemius and soleus muscle fibers and clarify the role of oxidative metabolism in the strenuous exercise-induced apoptosis. The experiment was designed with 49 (n = 49) male, 24-week-old, L. Wistar albino rats. Strenuous exercise model was applied to 42 (n = 42) rats and seven (n = 7) rats served as rested controls. All rats were randomly assigned to one of the following groups (n = 7): rested control (C), immediately after exercise (0 h) and 3, 6, 12, 24, and 48 h after exercise. Apoptotic nuclei were shown by single stranded DNA (ssDNA) determination. Oxidative damage in mitochondrial fractions of the muscle tissues was evaluated by malondialdehyde (MDA) levels and reduced/oxidized glutathione (GSH/GSSG) ratios. Caspase-9, -8 and -3 activities and the level of cytochrome c (Cyt c) were measured in the cytosolic fractions of muscle tissues to follow mitochondrial-dependent (intrinsic) or ligand-mediated death receptor (extrinsic) pathways of apoptosis. Plasma interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) levels were also determined. Based on our results, apoptosis is significantly triggered in muscle fibers by strenuous exercise (P < 0.05). Apoptosis in the soleus muscle tissues mostly depends on the intrinsic pathway and may be triggered by increased oxidative stress. In contrast, extrinsic pathway of apoptosis was predominant in the gastrocnemius muscle and increases of TNF-alpha and IL-6 may play a significant role.
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PMID:The apoptotic response to strenuous exercise of the gastrocnemius and solues muscle fibers in rats. 1803 Apr 91

Alleviative effects of histidine and carnosine in mice against ethanol-induced oxidative and inflammatory was examined. After chronic alcoholic liver injury was induced, histidine and carnosine at 0.5, 1, 2g/L were added to the drinking water for 3 weeks. Results showed that the post-intake of histidine or carnosine markedly decreased alanine aminotransferase and aspartate aminotransferase activities (P<0.05). Ethanol treatment increased malondialdehyde (MDA) level, decreased glutathione (GSH) content and catalase and glutathione peroxidase (GPX) activities, and increased cytochrome P450 2E1 (CYP2E1) activity in liver (P<0.05). The post-intake of histidine and carnosine significantly decreased MDA formations, increased GSH content, enhanced catalase and GPX activities, and suppressed CYP2E1 activity (P<0.05), in which the effects on catalase and CYP2E1 activities were dose-dependent (P<0.05). Ethanol treatment elevated hepatic levels of c-reactive protein (CRP), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) (P<0.05), the post-intake of histidine and carnosine significantly and dose-dependently diminished the release of CRP, IL-6, and TNF-alpha (P<0.05). Ethanol treatment caused down-regulation in both catalase and GPX mRNA expression, and up-regulated both IL-6 and TNF-alpha mRNA expression (P<0.05). Histidine and carnosine post-treatments significantly and dose-dependently upregulated catalase mRNA, and down-regulated mRNA expression of IL-6 and TNF-alpha (P<0.05). Based on the observed anti-oxidative and anti-inflammatory effects, the supplement of histidine or carnosine might be helpful for the treatment of chronic alcoholic liver injury.
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PMID:Beneficial effects of histidine and carnosine on ethanol-induced chronic liver injury. 1822 27

This experimental study investigated the antioxidant status of rats after resveratrol (R) treatment following 70% partial hepatectomy. Thirty Wistar albino rats (200 to 250 g) were divided among: groups A and B (n = 10 each) underwent laparotomy and 70% partial hepatectomy (PH). Whereas rats in group A received resveratrol 60 mg/d per nasogastric tube for 7 days before and 3 days after PH (PH + R), those in group B underwent PH only. Rats in group C (n = 10) were subjected to a sham operation. Significant increases in tissue levels of reduced glutathione (GSH) and decreased malondialdehyde (MDA) levels were observed in the PH group receiving R compared with those of the PH group (P < .001 for all). Comparison of these parameters with those of the sham group revealed significantly higher tissue levels of GSH and lower MDA levels among sham-operated compared with PH + R and PH groups (P < .001 for all). Concerning the NO levels, a trend to a slightly decrease was observed in the PH + R group (P < .06). Interleukin-6 levels showed significant decreases in both PH + R and PH groups (P < .001 and P < .05, respectively). The tissue GSH levels were slightly decreased in PH + R (P < .05), and decreased in the PH group compared with the controls (P = .002). We have suggested that patients undergoing living donor liver transplantation would likely benefit from prophylactic treatment with foods having resveratrol.
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PMID:Effect of resveratrol on oxidative stress enzymes in rats subjected to 70% partial hepatectomy. 1826 9


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