Nitric oxide as a mediator of inflammation?—You had better believe it

Miller, Mark J.S.; Grisham, Matthew B.

doi:10.1155/s0962935195000639

Cited by 64 publications

(45 citation statements)

References 17 publications

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“…However we detected a trace amount of the mass ions at m/z 48 and m/z 64 Da representing NO 2 -and NO 3 -with the inclusion of one 18 O atom. This experiment indicated that part of NO 2 -originated from RDX might also produce NO (31) which should subsequently auto-oxidize to revert back NO 2 -with one 18 O from water (32,33) prior to biological oxidation to NO 3 -(28). Results from the above H 2 18 O and 18 O 2 labeling experiments indicated that RDX denitration does not involve direct participation of either oxygen or water but both water and oxygen play major roles in the subsequent secondary chemical and biochemical reactions of the nitrite anion once released from RDX.…”

Section: Resultsmentioning

confidence: 99%

Biodegradation of RDX and MNX with Rhodococcus sp. Strain DN22: New Insights into the Degradation Pathway

Halasz

Manno

Strand

et al. 2010

Environ. Sci. Technol.

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Previously we demonstrated that Rhodococcus sp. strain DN22 can degrade RDX (hexahydro-1,3,5-trinitro-1,3,5-triazine) aerobically via initial denitration. The present study describes the role of oxygen and water in the key denitration step leading to RDX decomposition using 18 O 2 and H 2 18 O labeling experiments. We also investigated degradation of MNX (hexahydro-1-nitroso-3,5-dinitro-1,3,5-triazine) with DN22 under similar conditions. DN22 degraded RDX and MNX giving NO 2

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Section: Resultsmentioning

confidence: 99%

Biodegradation of RDX and MNX with Rhodococcus sp. Strain DN22: New Insights into the Degradation Pathway

Halasz

Manno

Strand

et al. 2010

Environ. Sci. Technol.

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“…Like COX-2, iNOS is a rapidly inducible enzyme that is expressed at sites of in¯ammation and injury in the gastrointestinal tract. 8 The dose of aspirin used in this study is suf®cient to cause profound suppression of systemic COX activity 27 and prostaglandin synthesis by the stomach. 32 It is therefore possible that the increase in COX-2 expression following aspirin administration occurred as a response to diminished tissue prostaglandin synthesis.…”

Section: Discussionmentioning

confidence: 95%

“…5±7 Nitric oxide synthase (NOS) is also constitutively expressed in the stomach, most notably in the endothelium (eNOS) and in enteric neurons (bNOS). 8 Inducible NOS (iNOS) can SUMMARY Background: Cyclo-oxygenase-1 (COX-1) is believed to produce prostaglandins vital to mucosal defence, whereas cyclo-oxygenase-2 (COX-2) is induced at sites of in¯ammation. Little is known about the regulation of COX-2 in the stomach, particularly during the period following mucosal injury.…”

Section: Introductionmentioning

confidence: 99%

Aspirin causes rapid up‐regulation of cyclo‐oxygenase‐2 expression in the stomach of rats

Davies

Sharkey

Asfaha

et al. 1997

Aliment Pharmacol Ther

125

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Background:Cyclo‐oxygenase‐1 (COX‐1) is believed to produce prostaglandins vital to mucosal defence, whereas cyclo‐oxygenase‐2 (COX‐2) is induced at sites of inflammation. Little is known about the regulation of COX‐2 in the stomach, particularly during the period following mucosal injury. In this study, we examined COX‐1 and COX‐2 expression shortly after administration of NSAIDs or ethanol.Methods:Fasted rats were given aspirin, salicylate, indomethacin or ethanol (20% or 40%) orally. Three hours later the stomach was excised, the severity of damage scored and samples taken for RT‐PCR of COX‐1 and COX‐2 mRNA and immunohistochemistry. Nitric oxide synthase mRNA (iNOS and eNOS) and activity were also measured.Results:Aspirin, indomethacin and the higher concentration of ethanol produced widespread mucosal damage, whereas salicylate and 20% ethanol caused only superficial epithelial damage. Aspirin caused a significant increase in COX‐2 mRNA expression and a marked increase in COX‐2 immunoreactivity, particularly in the superficial mucosa. Expression of COX‐1 (mRNA and protein) was unaffected by aspirin, as were NOS mRNA expression and enzyme activity. Pre‐treatment with prostaglandin E2 prevented the induction of COX‐2 by aspirin. Salicylate and indomethacin caused modest increases in COX‐2 immunoreactivity but no change in COX‐2 mRNA. Neither concentration of ethanol affected COX‐2 mRNA or protein expression, suggesting that this was a specific response to the aspirin, rather than to injury.Conclusions:These results demonstrate a rapid up‐regulation of COX‐2 expression in response to aspirin, possibly representing a compensatory response to inhibition of gastric prostaglandin synthesis.

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“…RAW 264.7 cells were mechanically scraped and plated at 1ϫ10 5 /well in 96-well plates containing 100 ml of RPMI 1640 medium with 10% FBS and incubated overnight. SCM was dissolved in DMSO, and the DMSO concentrations in all assays did not exceed 0.1%.…”

Section: Plant Materials and Preparation Of The Methanol Fractionmentioning

confidence: 99%

“…Studies have shown that the chronic phase of inflammation in particular correlates with an increase in iNOS activity. 5,6) The most conclusive evidence for NO as a mediator of tissue injury has been obtained from arthritis, which is based on studies in an animal model, human osteoarthritis, and rheumatoid arthritis. 7) The constitutive epithelial and neuronal forms of NOS contribute relatively little to inflammation and carcinogenesis.…”

mentioning

confidence: 99%

Inhibition of Methanol Extract from the Aerial Parts of Saururus chinensis on Lipopolysaccharide-Induced Nitric Oxide and Prostagladin E2 Production from Murine Macrophage RAW 264.7 Cells.

Kim

Shin

Kim

et al. 2003

Biological & Pharmaceutical Bulletin

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As an attempt to search for bioactive natural products exerting antiinflammatory activity, we have evaluated the effects of the methanol extract from the aerial parts of Saururus chinensis (LOUR.) BAILL (Saururaceae) on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E 2 (PGE 2 ) release by the macrophage cell line RAW 264.7. Our data indicate that this extract is a potent inhibitor of NO production and it also significantly decreased PGE 2 release. Consistent with these observations, the protein and mRNA expression level of inducible NO synthase (iNOS) and cyclooxygenase (COX)-2 was inhibited by MeOH extracts of the aerial part of S. chinensis (SCM) in a dose-dependent manner. Furthermore, SCM inhibited the LPS-induced DNA binding activity of nuclear factor-k kB (NF-k kB), which was associated with decreased p65 protein levels in the nucleus. These results suggest that SCM inhibits LPS-induced iNOS and COX-2 expression by blocking NF-k kB activation.

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Nitric oxide as a mediator of inflammation?—You had better believe it

Cited by 64 publications

References 17 publications

Biodegradation of RDX and MNX with Rhodococcus sp. Strain DN22: New Insights into the Degradation Pathway

Biodegradation of RDX and MNX with Rhodococcus sp. Strain DN22: New Insights into the Degradation Pathway

Aspirin causes rapid up‐regulation of cyclo‐oxygenase‐2 expression in the stomach of rats

Inhibition of Methanol Extract from the Aerial Parts of Saururus chinensis on Lipopolysaccharide-Induced Nitric Oxide and Prostagladin E2 Production from Murine Macrophage RAW 264.7 Cells.

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