Prevention by L-Arginine/Nitric Oxide of Chlordiazepoxide-Induced Toxic Reactions in the Rat Salivary Gland

Ahmed, Abdollah Osman; Sharifzadeh, Mohammad; Nikfar, Shekoufeh; Jamshidi, Hamid Reza; Abdollahi, Mohammad

doi:10.1080/15376520600620067

Cited by 3 publications

(1 citation statement)

References 54 publications

(54 reference statements)

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“…One promising mechanism might be the involvement of NO, an endogenous mediator that not only has indispensable physiological roles but also shows various toxic effects [51][52][53]. Several investigations have shown that in acute colitis constitutive production of NO from endothelial NO synthase (eNOS) is advantageous, but chronic overproduction of NO through activation of inducible NOS (iNOS) is associated with progression of inflammation and tissue injury [53,54].…”

Section: Discussionmentioning

confidence: 99%

Benefit of nicorandil using an immunologic murine model of experimental colitis

et al. 2009

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Inflammatoryboweldisease(IBD)isachronicinflammatoryconditionwithanunknownetiology.Nicorandil,apotassiumchannel opener, has been used for many years for the treatment of angina. Recently, it has been shown that nicorandil possesses some novel traits such as anti-apoptotic, gastroprotective, free radical scavenging, and anti-inflammatory properties. Therefore, we set out to examine the possible beneficial effect of nicorandil in a rat model of IBD. Colitis was induced by rectal administration of 2,4,6-trintrobenzene sulphonic acid (TNBS) into rats. Groups of animals used in this study were sham, control, and exposure to dexamethasone,nicorandil,glibenclamid(apureadenosinetriphosphatesensitivepotassiumchannel(KATP)blocker),ornicorandilplus glibenclamid.Drugswereadministeredbygavageandanimalsweresacrificedafter7days.Biochemicalmarkers,includingTNF-αand IL-1β,ferricreducing/antioxidantpower(FRAP),myeloperoxidase(MPO)activityandthiobarbitoricacid-reactivesubstance(TBARS), weremeasuredinthehomogenateofcolonictissue.Resultsindicatethatnicorandilsignificantlyreducesmacroscopicandhistological damageinducedbyTNBS.NicorandildiminishesMPOactivityandlevelsofTBARS,TNF-α,andIL-1βindamagedcolonictissuewith aconcomitantincreaseinFRAPvalue(P<0.01).Theseeffectswerenotreversedbycoadministrationofglibenclamide.Inconclusion, nicorandilisabletoameliorateexperimentalIBDwithadoseinwhichitdoesnotshowanyanti-hypertensiveeffect,andthemechanism ofwhichispartiallyortotallyindependentfromKATPchannels.Itishypothesizedthatnitricoxidedonationandfree-radicalscavenging propertiesofnicorandilupregulateendothelialnitricoxidesynthasemayberesponsibleforthisphenomenon.Thesefindingssuggest thatnicorandilcanbeusefulintreatmentofIBD,althoughfurtherinvestigationsareneededtoelucidatethemechanismsinvolved.

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Section: Discussionmentioning

confidence: 99%

Benefit of nicorandil using an immunologic murine model of experimental colitis

et al. 2009

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Monitoring the biochemical alterations in hypertension affected salivary gland tissues using Fourier transform infrared hyperspectral imaging

Nazeer

Samrid

Pérez-Guaita

et al. 2017

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Fourier transform infrared spectroscopy (FTIR) imaging has been applied to investigate biochemical differences between salivary glands from control and hypertensive rats. Male Sprague-Dawley rats were divided into two groups including a control group and another hypertension group that were treated orally, with N-nitro-l-arginine methyl ester (l-NAME) via drinking water for 3 weeks to develop hypertension. In the control group, rats were treated with only drinking water for 3 weeks. The formalin-fixed paraffin embedded tissue specimens from submandibular and sublingual glands were analysed with a FTIR focal plane array imaging spectrometer and multi-composite images of all tissue sections were analysed simultaneously using Unsupervised Hierarchical Cluster Analysis (UHCA) and the extracted spectra were further analysed using Partial Least Squares Discriminant Analysis (PLS-DA). In general, hypertension affected salivary gland tissues were characterised by higher concentrations of triglycerides as evidenced by an increase in the 1745 cm band. Higher concentrations of carbohydrates and proteins were also observed in the hypertensive group along with a decrease in bands associated with nucleic acids. PLS-DA scores plots provided good differentiation in sublingual gland tissues between control (n = 3734 spectra) and hypertension (n = 4538) and also in submandibular gland tissues between control (n = 5051) and hypertension (n = 4408). We have shown that FTIR imaging can be used to differentiate the macromolecular information between physiological and pathological conditions in tissue biopsy specimens. In the next phase, we will investigate the infrared predictive markers of hypertension in biofluids including serum and saliva using attenuated total refection spectroscopy.

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Restoration of morphine-induced alterations in rat submandibular gland function by N-methyl-D-aspartate agonist

Hashemi¹,

Mohammadirad²,

Bayrami³

et al. 2006

Acta Biologica Hungarica

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The effects of morphine, 1-aminocyclobutane-cis-1,3-dicarboxylic (ACBD; NMDA agonist) and 3-((R)2-carboxypiperazin-4-yl)-propyl-l-phosphoric acid (CPP; NMDA antagonist) and their concurrent therapy on rat submandibular secretory function were studied. Pure submandibular saliva was collected intraorally by micro polyethylene cannula from anaesthetized rats using pilocarpine as secretagogue. Intraperitoneal injection of morphine (6 mg/kg) induced significant inhibition of salivary flow rate, total protein, calcium, and TGF-beta1 concentrations. Administration of ACBD (10 mg/kg) and CPP (10 mg/kg) alone did not influence secretion of submandibular glands. In combination therapy, coadministration of CPP with morphine did not influence morphine-induced changes in salivary function while ABCD could restore all morphine-induced changes. In combination treatment, ACBD prevented morphine-induced reduction of flow rate, total protein, calcium, and TGF-beta1 and reached control levels. It is concluded that morphine-induced alterations in submandibular gland function are mediated through NMDA receptors.

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Prevention by L-Arginine/Nitric Oxide of Chlordiazepoxide-Induced Toxic Reactions in the Rat Salivary Gland

Cited by 3 publications

References 54 publications

Benefit of nicorandil using an immunologic murine model of experimental colitis

Benefit of nicorandil using an immunologic murine model of experimental colitis

Monitoring the biochemical alterations in hypertension affected salivary gland tissues using Fourier transform infrared hyperspectral imaging

Restoration of morphine-induced alterations in rat submandibular gland function by N-methyl-D-aspartate agonist

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