Adrenergic Regulation of Prostaglandin Biosynthesis in Cultured Rabbit Gastric Epithelial Cells.

Ueda, Fusao; Ideguchi, Kyoichi; Taniguchi, N; Kimura, Kiyoshi

doi:10.1254/jjp.65.113

Cited by 7 publications

(6 citation statements)

References 23 publications

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“…This study also demonstrated the interaction between the sympathetic system and COX‐2, as β ‐blockade treatment normalized the overexpressed COX‐2 in gastric tissues of burned rats. This was consistent with previous studies . Taken together, these findings suggest that sympathetic hyperactivity may mediate burn‐induced delay in gastric emptying either directly or via the COX‐2 pathway.…”

Section: Discussionsupporting

confidence: 92%

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Auricular vagal nerve stimulation ameliorates burn‐induced gastric dysmotility via sympathetic‐COX‐2 pathways in rats

Yin

Zhang

et al. 2015

Neurogastroenterology Motil

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BACKGROUND & AIMS Severe burn injury has been demonstrated to delay gastric emptying. The aim of this study was to investigate effects and cellular mechanisms of auricular electroacupuncture (AEA) at the acupoints innervated by the auricular branch of vagus nerve (ABVN) on burn-induced gastric dysmotility in rats. METHODS Propranolol (β-adrenoceptor antagonist) was injected intraperitoneally after the rats underwent burn injury. All experiments were performed six hours following burn/sham burn injury. AEA was performed at bilateral auricular acupoints for 45min. Electrocardiogram was recorded for 30min. Plasma hormones were measured; cyclooxygenase (COX)-2 expressions in gastric tissue were measured using western blotting and real time RT-PCR. RESULTS 1) Burn injury delayed gastric emptying (P=0.006) and AEA increased gastric emptying by 49% (P=0.045). 2) Burn injury evoked a significant elevation in plasma noradrenaline, which was suppressed by AEA. 3) Burn injury significantly increased protein and mRNA expressions of COX-2 in gastric fundus and antrum. AEA suppressed burn-induced increase in protein expressions but not mRNA expressions of COX-2. CONCLUSIONS Burn injury delays gastric emptying by up-regulating COX-2 attributed to sympathetic overactivity. AEA improves burn-induced delay in gastric emptying, possibly mediated via the sympathetic-COX-2 pathway.

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Section: Discussionsupporting

confidence: 92%

“…This was consistent with previous studies. 33,34 Taken together, these findings suggest that sympathetic hyperactivity may mediate burn-induced delay in gastric emptying either directly or via the COX-2 pathway.…”

Section: Discussionmentioning

confidence: 83%

Auricular vagal nerve stimulation ameliorates burn‐induced gastric dysmotility via sympathetic‐COX‐2 pathways in rats

Yin

Zhang

et al. 2015

Neurogastroenterology Motil

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“…Previous study, similarly to our present report, demon strated that the direct stimulation of P-adrcnoceptors with ISO significantly protected gastric mucosa against the damage by ethanol [3,5,[22][23][24] and stress [20] and that this could be attributed, at least in part, to the enhance ment in mucus and phospholipid secretion [3,4] strength ening gastric mucosal defense [3,4,22].…”

Section: Discussionsupporting

confidence: 90%

Role of β-Adrenoceptors in Gastric Mucosal Integrity and Gastroprotection Induced by Epidermal Growth Factor

et al. 1997

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The central and peripheral adrenergic systems are involved in the regulation of gastric secretion but little is known about the role of α- and β-adrenoceptors in gastroprotection. In this study, acute gastric lesions were produced by an intragastric (i.g.) application of 100% ethanol and gastric blood flow (GBF) was determined by H₂-gas clearance technique in rats with or without i.g. or intraperitoneal (i.p.) administration of α- or β-adrenoceptor agonists or antagonists. Phenylephrine, α₁-adrenergic agonist, and clonidine, α₂-agonist, significantly augmented the ethanol-induced lesions while decreasing the GBF and these effects were reversed by the blockade of α₁-adrenoceptors with prazosin and α₂-adrenoceptors with yohimbine. In contrast, isoproterenol (ISO) (0.01-10 mg/kg i.g.), β-adrenoceptor agonist, reduced dose-dependently ethanol-induced mucosal injury and this effect was accompanied by an elevation of the GBF similarly as after epidermal growth factor (EGF) (100 μg/kg·h s.c.) or after classic protective agent, 16,16-dimethyl-PGE₂ (PGE₂) (10 μg/kg i.g.). The pretreatment with β-antagonist, propranolol, diminished the protective and hyperemic effects of ISO and EGF but failed to affect those induced by PGE₂. Suppression of nitric oxide (NO) synthase activity by L-NAME or sensory denervation with capsaicin attenuated significantly the ISO- and EGF-induced gastroprotection and elevation of GBF, whereas the inhibition of PG biosynthesis by indomethacin remained without any significant effect. Adrenal medullectomy or chemical sympathectomy by 6-hydroxydopamine by itself failed to influence significantly the ethanol-induced damage but completely abolished the protective and hyperemic effects of EGF being without any influence on those induced by PGE₂. ISO combined with EGF, restored the protective and hyperemic effects of this peptide in medullectomized rats. We conclude that (1) local activation of β-adrenoceptors by ISO affords protection and elevation of GBF, both these effects being mediated by arginine-NO pathway and sensory nerves and (2) sympathetic system and adrenal medulla contribute to the protective and hyperemic activity of EGF.

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“…A complex relationship exists between CAs and PGs. There are reports that high CA levels can cause the release of PGs (Ueda et al 1994), and that PGs can induce the release of CAs (Yokotani et al 1995). In addition, it was found that pretreatment with indomethacin suppressed the increase in CAs induced by LPS (Sakata et al 1994).…”

Section: Discussionmentioning

confidence: 99%

Metastatic-promoting effects of LPS: Sexual dimorphism and mediation by catecholamines and prostaglandins

Naor¹,

Domankevich²,

Shemer³

et al. 2009

Brain, Behavior, and Immunity

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Inflammation is implicated in several medical conditions that are sexually dimorphic, including depression, cardiovascular diseases, autoimmunity, and presumably cancer progression. Here we studied the effects of the pro-inflammatory agent, LPS, on MADB106 lung tumor retention (LTR), and sought to elucidate underlying mechanisms and sexual dimorphism. F344 male and female rats were administered with LPS (0.001-1 mg/kg i.v.) simultaneously with tumor cell inoculation, and treated with a β-blocker (nadolol, 0.2-0.3 mg/kg s.c.), a COX-inhibitor (indomethacin, 4 mg/kg s.c.) or both drugs. To study the role of NK cells, numbers and cytotoxicity of marginating-pulmonary NK cells were studied, and selective in vivo NK-depletion was employed. Serum levels of corticosterone, IL-6, and TNF-α were also assessed. The findings indicated that LPS increased LTR in both sexes, but 10-fold higher doses were needed in females to reach the increase evident in males. Additionally, nadolol and indomethacin reduced the effects of LPS, more so in males. In vivo NKdepletion and ex-vivo NK activity studies suggested that LPS affected LTR through both NKindependent and NK-dependent mechanisms, the latter mediated through prostaglandin release in males. Corticosterone, IL-6, and TNF-α responses to LPS were sexually dimorphic, but were not associated with LPS or drugs' impacts on LTR. Overall, our findings demonstrate sexual dimorphism in LPS-induced elevated susceptibility to MADB106 experimental metastasis, and in potential humoral underlying mechanisms. Further studies are needed to elucidate additional immunological and non-immunological mediators of these dimorphisms, as well as to assess their involvement in other sexually dimorphic pathologies that are associated with inflammation.

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Adrenergic Regulation of Prostaglandin Biosynthesis in Cultured Rabbit Gastric Epithelial Cells.

Cited by 7 publications

References 23 publications

Auricular vagal nerve stimulation ameliorates burn‐induced gastric dysmotility via sympathetic‐COX‐2 pathways in rats

Auricular vagal nerve stimulation ameliorates burn‐induced gastric dysmotility via sympathetic‐COX‐2 pathways in rats

Role of β-Adrenoceptors in Gastric Mucosal Integrity and Gastroprotection Induced by Epidermal Growth Factor

Metastatic-promoting effects of LPS: Sexual dimorphism and mediation by catecholamines and prostaglandins

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