Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 4

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
Experimental and clinical gastrointestinal data reported that nitrosative stress development involved in impaired barrier function, altered motility and a lowered threshold to noxious stimuli, but its pathogenetic role in diabetic esophagopathy remains unexplored. We tested the hypothesis that an imbalance in nonenzymatic glycation and glycooxidation, enhanced peroxynitrite formation, may play an important role in development esophageal mucosa (EM) lesions during streptozotocin-induced experimental hyperglycemia (EHG). To understand the biological significance of EM resistance in vivo used a glycomic approach to identification of lectin receptors glycosylation pattern. Were enrolled rat groups without/with EHG & modification of NO/NOS activity by L-arginine (L-arg) and indomethacin pre-treatment. Survival rate, destruction occurrence ratio, the size of EM lesions, and the number of EM lesions was investigated. To access the oligosaccharide residues the peroxidaseconjugated lectin (HPA, SNA, WGA, PNA)-diaminobenzidine procedure was performed to EM sections. EHG was monitored daily by glucometer. Content of NO (NOn) was determinated by Griess reagent and reactive oxygen-scavenging systems (ROSS) activity - generally accepted biochemical methods. In EHG and L-arg pretreatment group reduced NOn and EM injury with markedly rise ROSS activity significantly vs to control; in the group with indomethacin pretreatment existed different ROSS activity. Presence of heterogeneous glycosylation pattern in different layers of EM was shown. In EHG staining with PNA and SNA were strongly positive. NS and ROSS play a critical role in esophagoprotection induced by EHG, because both involved increases in iNOS expression. These results indicate the usefulness of glycomic approach as multifunctional substrate of early evaluation of NS in esophageal physiopathy.
Melatonin (MT) is known to protect gastrointestinal mucosa against various types of injury but its effects on esophageal damage have not been studied. We examined the effects of MT on acute esophageal injury and the mechanism involved in the action of this indole. Acute esophageal lesions were induced by perfusion with acid-pepsin solution using tube inserted through the oral cavity into the mid of esophagus of anaesthetized rats with or without inhibition of prostaglandin (PG) generation by indomethacin (5 mg/kg/day), nitric oxide (NO) formation by NG-nitro-L-arginine (L-NNA, 20 mg/kg/day) or sensory nerves deactivation by capsaicin (125 mg/kg, sc). The esophageal injury was assessed by macroscopic score and histologic activity index. The esophageal mucosal blood flow (EBF) was determinated by H2-gas clearance method. The plasma TNF-alpha and nitrate/nitrite (NOx) levels and mucosal PGE2 contents were assessed by immunoassays. Esophageal acid-pepsin perfusion induced noticeable esophageal mucosal injury as compared to perfusion with vehicle saline. The pretreatment with MT prevented significantly esophageal injury, raised EBF and mucosal content of PGE2, while decreasing the levels of TNF-alpha. Inhibition of COX/PG and NOS/NO systems by indomethacin and L-NNA, respectively, or inactivation of sensory nerves by capsaicin, that manifested in further increase of esophageal injury, reduced the levels of EBF, markedly raised the levels TNF-alpha and reduced mucosal PGE2, but the pretreatment with MT prevented significantly esophageal injury, improved EBF and raised mucosal PGE2 contents. These studies suggest that MT can be considered as a novel esophagoprotector, acting, at least in part, through the COX/PG and NOS/NO systems and activation of sensory nerves.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.