الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
This study comprised 80 adult male albino rats .They were divided into four groups:Group I (control group): rats given distilled water 35 mg/kg subcutaneously.Group II (Indomethacin treated group): rats received indomethacin subcutaneously as a single dose of 35 mg/kg body.Group III (Indomethacin and LNAME treated rats): rats received LName (NG nitroLarginine methyl ester) intraperitoneally at a dose of 50 mg/kg half an hour before giving indomethacin.Group IV (Indomethacin and LNIL treated rats): rats were given LNIL (N6(iminoethyl)Llysine) intraperitoneally at a dose of 3 mg/kg half an hour before giving indomethacin .The animals were sacrified. The specimens were assessed by dissecting microscope and then stained by haematoxylin, eosin, and immunohistochemical staining for the endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS). Immunohistochemically stained sections were submitted for the image analysis. Aim of the work The aim of this study is to explore the role of nitric oxide synthases (NOSs) inhibitors (LNAME) (nonselective endothelial NOS/inducible NOS (eNOS/iNOS) inhibitor) and (LNIL) (selective iNOS) in the pathogenesis of indomethacin induced gastric mucosal lesions. Results In the control group, macroscopic and histological examination revealed normal appearance of the gastric mucosa. Expression of iNOS was less than with eNOS in normal gastric mucosa. In indomethacinadministrated group, macroscopic and histological examination revealed timedependent occurrence of damage in the stomach from 6 hours up to 72 hour. Statistical results obtained by image analyzer revealed that expression of iNOS was more than eNOS. In indomethacin and LNAME administrated group, there was increase in gastric mucosal lesions. It was observed that expression of iNOS was more than that in indomethacin given group or control group. Also iNOS immunoreactivity was higher than eNOS immunoreactivity in this group. In indomethacin and LNIL administrated group, pretreatment with LNIL reduced but not prevented gastric mucosal lesions induced by indomethacin. There was time course increase in eNOS immunoreactivity from 6 hours until 72 hours reaching its maximum level on 48 hours and 72 hours and time course decrease in iNOS immunoreactivity from 6 hours until 72 hours reaching its minimum level on the third day. eNOS immunoreactivity was higher than iNOS immunoreactivity in this group. Summary and Conclusion In rats treated with indomethacin, a decrease in gastric mucosal eNOS activity and an increase in gastric mucosal iNOS activity were closely related to the development of gastric mucosal lesions. it could be concluded that inhibition of NOS could have either beneficial or deleterious effects on gastric injury, depending on which isoform is being inhibited.