Ulcer healing in diabetic rats treated with aspirin, nitric oxide (NO)-derivative of aspirin and COX-2 inhibitor

Brzozowski, T; Konturek, Peter C.; Śliwowski, Zbigniew; Pawlik, Michał; Stachura, Jerzy; Konturek, Stanisław J.; Jaworek, Jolanta; Pawlik, Wiesław W.; Hahn, Eckhart G.

doi:10.1016/s0016-5085(03)80850-8

Cited by 33 publications

(42 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Twice-daily injections of aspirin (2 × 15 mg/kg) and flurbiprofen (2 × 3 mg/kg) were sufficient to saturate the tissues and, unquestionably, to systemically inhibit the COX. The particular doses used in this study were supported by the literature (30). Even when strong survival endpoints were not statistically reached, test drugs were absorbed, since NCX 4016 displayed some limited benefit and flurbiprofen was able to produce fibrosis, necrosis, and spleen enlargement.…”

Section: Discussionsupporting

confidence: 56%

The effects of aspirin, flurbiprofen, and NO-donating acetylsalicylic acid(NCX 4016) on mice models of endotoxic and septic shock

Ulu¹,

İskit

Sökmensüer³

et al. 2015

Turk J Med Sci

View full text Add to dashboard Cite

Background/aim: Nitric oxide-donating nonsteroidal antiinflammatory drugs (NO-NSAIDs) are a promising new class of antiinflammatory agents, which are obtained by adding NO-donating moieties to the existing conventional NSAID molecules. The aim of this study was to investigate the effects of aspirin, flurbiprofen, and NO-donating acetylsalicylic acid (NCX 4016) on cecal ligation and puncture (CLP) and endotoxin-induced septic shock (LPS) models in mice. Materials and methods:Overall survival and spleen and liver weights were monitored in LPS and CLP models. Histopathological examinations of liver and spleen were performed at the end of the experimental protocols.Results: NCX 4016 was able to reverse the increased spleen weight in CLP-operated animals, whereas aspirin or flurbiprofen did not. Similar to the results of the CLP model, none of the drugs modified the survival rates in the LPS model. Flurbiprofen in particular produced significant histopathological damage in spleens and livers, which was less significant with aspirin. NCX 4016 did not cause any liver damage. Conclusion:NCX 4016 has the potential to be used in septic states, while special attention has to be paid to the effects of aspirin and flurbiprofen on the liver and spleen.

show abstract

Section: Discussionsupporting

confidence: 56%

The effects of aspirin, flurbiprofen, and NO-donating acetylsalicylic acid(NCX 4016) on mice models of endotoxic and septic shock

Ulu¹,

İskit

Sökmensüer³

et al. 2015

Turk J Med Sci

View full text Add to dashboard Cite

show abstract

“…PTX decreased the levels of TNF-α and IL-1β significantly in EtOH-induced ulcerated gastric mucosa, and the above observation is in confirmation with the reported work of other workers. [2,23,24] TNF-α is reported to stimulate the upregulation of IL-1β levels, so by controlling the TNF-α expression, the IL-1β expression can be controlled. This may be the mechanism by which PTX decreases both the cytokines levels.…”

Section: Discussionmentioning

confidence: 99%

Status of inflammatory markers and growth factor in gastric ulcer protective effects of Punica granatum L. peel extract in rat

Chauhan¹,

Agrawal²,

Goel³

2018

Natl J Physiol Pharm Pharmacol

View full text Add to dashboard Cite

Background: Inflammatory markers, namely, myeloperoxidase (MPO), cytokines (tumor necrosis factor-alpha [TNF-α], and interleukin-1 beta ) and vascular endothelial growth factor (VEGF) have been reported to play an important role in ulcerogenesis and healing. Recently, we reported that the gastric ulcer (GU) protective and healing effects of 50% ethanol (EtOH) extract of Punica granatum peel (PGE) in rats were predominantly due to strengthening of mucosal defense and antioxidants status. Aims and Objectives: The present study incorporates the effects of PGE on rat gastric mucosal inflammatory markers (MPO, TNF-α, and IL-1β) and angiogenic factor (VEGF) in GU induced by cold-restraint stress (CRS) and EtOH in rats. Materials and Methods: PGE (100 mg/kg) was administered orally once daily to rats for 7 days before induction of CRS and EtOH GU. Ulcer index (UI), gastric mucosal MPO, TNF-α, and IL-1β, and VEGF were estimated. Results: CRS rats showed increase in UI and MPO (419.5, P < 0.001) compared with unstressed rats while PGE caused decrease in UI (46.1%, P < 0.05) and MPO (51.1%, P < 0.001) compared with CRS rats. EtOH rats showed increase in UI, TNF-α (936.5%, P < 0.001), IL-1β (37.2%, P < 0.05), and VEGF (13.0%, P < 0.05) compared with control normal salinetreated rats. PGE-treated EtOH rats showed decrease in UI (68.9%, P < 0.05), TNF-α (77.9%, P < 0.01), and IL-1β (24.8%, P < 0.05) but tended to decrease VEGF (7.3%, P < 0.2) compared with EtOH rats. Conclusion: Both the inflammatory markers and VEGF were found to increase in GU rats while PGE EtOH extract decreased the status of inflammatory markers with little change in VEGF level with concomitant decrease in ulceration indicating their role in ulcer healing and repair.

show abstract

“…49 -51 This is in accord with other studies that have shown that activation of capsaicin-sensitive neurons plays an important role in protecting ischemic bowel viability. [52][53][54] Because blockade of NK 1 receptor, but not CGRP receptor, reversed the protective effect on mucosal damage induced by exogenous activation of PAR 2 , it is reasonable to suggest that the PAR 2 -protective effect is at least in part mediated by SP released from visceral afferents. By contrast, CGRP does not appear to play an important role in this protective effect.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Proteinase-Activated Receptor 2 Activation on Motility Impairment and Tissue Damage Induced by Intestinal Ischemia/Reperfusion in Rodents

Cattaruzza

Cenac

Barocelli

et al. 2006

The American Journal of Pathology

View full text Add to dashboard Cite

We hypothesized that proteinase-activated receptor-2 (PAR 2 ) modulates intestinal injuries induced by ischemia/reperfusion. Ischemia (1 hour) plus reperfusion (6 hours) significantly delayed gastrointestinal transit (GIT) compared with sham operation. Intraduodenal injection of PAR 2 -activating peptide SLIGRL-NH 2 significantly accelerated transit in ischemia/reperfusion but not in sham-operated rats. GIT was significantly delayed in ischemia/reperfusion and sham-operated PAR 2 ؊/؊ mice compared with PAR 2 ؉/؉ . SLIGRL-NH 2 significantly accelerated transit in ischemia/reperfusion in PAR 2 ؉/؉ but not in PAR 2 ؊/؊ mice. Prevention of mast cell degranulation with cromolyn, ablation of visceral afferents with capsaicin, and antagonism of calcitonin generelated peptide (CGRP) and neurokinin-1 receptors with CGRP 8 -37 and RP67580, respectively, abolished the SLIGRL-NH 2 -induced stimulatory effect on transit in ischemia/reperfusion. Tissue damage was significantly reduced by SLIGRL-NH 2 ; this effect was not observed in cromolyn-, capsaicin-, or RP67580-treated rats but was detected following CGRP 8 -37 . Intestinal PAR 2 mRNA levels were not affected by SLIGRL-NH 2 in ischemia/reperfusion. We propose that PAR 2 modulates GIT and tissue damage in intestinal ischemia/reperfusion by a mechanism dependent on mast cells and visceral afferents. PAR 2 effect on transit might be mediated by CGRP and substance P, whereas the effect on tissue damage appears to involve substance P but not CGRP. PAR 2 might be a signaling system in the neuroimmune communication in intestinal ischemia/reperfusion.

show abstract

Ulcer healing in diabetic rats treated with aspirin, nitric oxide (NO)-derivative of aspirin and COX-2 inhibitor

Cited by 33 publications

References 0 publications

The effects of aspirin, flurbiprofen, and NO-donating acetylsalicylic acid(NCX 4016) on mice models of endotoxic and septic shock

The effects of aspirin, flurbiprofen, and NO-donating acetylsalicylic acid(NCX 4016) on mice models of endotoxic and septic shock

Status of inflammatory markers and growth factor in gastric ulcer protective effects of Punica granatum L. peel extract in rat

Protective Effect of Proteinase-Activated Receptor 2 Activation on Motility Impairment and Tissue Damage Induced by Intestinal Ischemia/Reperfusion in Rodents

Contact Info

Product

Resources

About